Mitochondrial Transplantation: A Novel Therapeutic Approach for Treating Diseases

Xinglu Miao , Pei Jiang , Zhaoping Wang , Weihua Kong , Lei Feng

MedComm ›› 2025, Vol. 6 ›› Issue (6) : e70253

PDF
MedComm ›› 2025, Vol. 6 ›› Issue (6) :e70253 DOI: 10.1002/mco2.70253
REVIEW

Mitochondrial Transplantation: A Novel Therapeutic Approach for Treating Diseases

Author information +
History +
PDF

Abstract

Advances in mitochondrial biology have led to the development of mitochondrial transplantation as a novel and promising therapeutic strategy. This review provides a comprehensive analysis of the multifaceted roles of mitochondria in health and disease, highlighting their central functions in energy production, antioxidant defense, calcium signaling, apoptosis regulation, and mitochondrial homeostasis maintenance. We explore the mechanisms by which transplanted mitochondria exert their therapeutic effects, including restoring ATP production, attenuating oxidative stress, modulating inflammatory responses, reducing cellular apoptosis, promoting cell repair and regeneration, facilitating neural circuit reconstruction, and exhibiting antitumor properties. Key preclinical studies demonstrating the efficacy of mitochondrial transplantation across in vitro and in vivo disease models are discussed, along with the status of clinical trials. The review also critically compares mitochondrial transplantation with other mitochondria-targeted therapies, evaluating their relative advantages and limitations. Finally, we discuss the current challenges of translating this innovative therapy into clinical practice, such as mitochondrial isolation and purification, storage, targeted delivery, potential immune responses, and long-term safety and efficacy concerns. This review aims to stimulate further research and development in this promising field, paving the way for novel therapeutic interventions for various diseases.

Keywords

disease therapy / mitochondria / mitochondrial transplantation / therapeutic strategy

Cite this article

Download citation ▾
Xinglu Miao, Pei Jiang, Zhaoping Wang, Weihua Kong, Lei Feng. Mitochondrial Transplantation: A Novel Therapeutic Approach for Treating Diseases. MedComm, 2025, 6(6): e70253 DOI:10.1002/mco2.70253

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

D. C. Chan, “Mitochondria: Dynamic Organelles in Disease, Aging, and Development,” Cell 125, no. 7 (2006): 1241-1252.

[2]

C. Wang and R. J. Youle, “The Role of Mitochondria in Apoptosis,” Annual Review of Genetics 43 (2009): 95-118.

[3]

M. P. Bordone, M. M. Salman, H. E. Titus, et al., “The Energetic Brain—A Review From Students to Students,” Journal of Neurochemistry 151, no. 2 (2019): 139-165.

[4]

M. R. Duchen, A. Verkhratsky, and S. Muallem, “Mitochondria and Calcium in Health and Disease,” Cell Calcium 44, no. 1 (2008): 1-5.

[5]

W. F. Graier, M. Frieden, and R. Malli, “Mitochondria and Ca (2+) Signaling: Old Guests, New Functions,” Pflügers Archiv - European Journal of Physiology 455, no. 3 (2007): 375-396.

[6]

W. Li, X. Liao, K. Lin, et al., “Earlier Second Polar Body Transfer and Further Mitochondrial Carryover Removal for Potential Mitochondrial Replacement Therapy,” MedComm 4, no. 3 (2023): e217.

[7]

Y. Zong, H. Li, P. Liao, et al., “Mitochondrial Dysfunction: Mechanisms and Advances in Therapy,” Signal Transduction and Targeted Therapy 9, no. 1 (2024): 124.

[8]

J. S. Harrington, S. W. Ryter, M. Plataki, et al., “Mitochondria in Health, Disease, and Aging,” Physiological Reviews 103, no. 4 (2023): 2349-2422.

[9]

A. Beckers and L. Moons, “Dendritic Shrinkage After Injury: A Cellular Killer or a Necessity for Axonal Regeneration?,” Neural Regeneration Research 14, no. 8 (2019): 1313.

[10]

F. Sayehmiri, F. Motamedi, Z. Batool, et al., “Mitochondrial Plasticity and Synaptic Plasticity Crosstalk; in Health and Alzheimer's Disease,” CNS Neuroscience & Therapeutics 30, no. 8 (2024): e14897.

[11]

A. Mandal and C. M. Drerup, “Axonal Transport and Mitochondrial Function in Neurons,” Frontiers in Cellular Neuroscience 13 (2019): 373.

[12]

K. A. Cojocaru, I. Luchian, A. Goriuc, et al., “Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease,” Antioxidants (Basel) 12, no. 3 (2023): 658.

[13]

Y. Zhang, L. Zhou, G. Cheng, et al., “Cordyceps sinensis Ameliorates Idiopathic Pulmonary Fibrosis in Mice via Inhibiting Mitochondrion-mediated Oxidative Stress,” MedComm - Future Medicine 3, no. 3 (2024): e91.

[14]

M. M. Khan, H. G. Paez, C. R. Pitzer, and S. E. Alway, “The Therapeutic Potential of Mitochondria Transplantation Therapy in Neurodegenerative and Neurovascular Disorders,” Current Neuropharmacology 21, no. 5 (2023): 1100-1116.

[15]

A. Celik, A. Orfany, J. Dearling, et al., “Mitochondrial Transplantation: Effects on Chemotherapy in Prostate and Ovarian Cancer Cells in Vitro and in Vivo,” Biomedicine & Pharmacotherapy 161 (2023): 114524.

[16]

B. Mokhtari, M. Hamidi, R. Badalzadeh, and A. Mahmoodpoor, “Mitochondrial Transplantation Protects Against sepsis-induced Myocardial Dysfunction by Modulating Mitochondrial Biogenesis and Fission/Fusion and Inflammatory Response,” Molecular Biology Reports 50, no. 3 (2023): 2147-2158.

[17]

J. H. Park, M. Tanaka, T. Nakano, et al., “O-GlcNAcylation Is Essential for Therapeutic Mitochondrial Transplantation,” Communications Medicine 3, no. 1 (2023): 169.

[18]

Y. Yin and H. Shen, “Common Methods in Mitochondrial Research (Review),” International Journal of Molecular Medicine 50, no. 4 (2022): 126.

[19]

W. B. Hubbard, C. L. Harwood, P. Prajapati, et al., “Fractionated Mitochondrial Magnetic Separation for Isolation of Synaptic Mitochondria From Brain Tissue,” Scientific Reports 9, no. 1 (2019): 9656.

[20]

R. Acin-Perez, C. Benincá, B. Shabane, et al., “Utilization of Human Samples for Assessment of Mitochondrial Bioenergetics: Gold Standards, Limitations, and Future Perspectives,” Life 11, no. 9 (2021): 949.

[21]

M. Bonora, S. Patergnani, A. Rimessi, et al., “ATP Synthesis and Storage,” Purinergic Signal 8, no. 3 (2012): 343-357.

[22]

M. Rigoulet, C. L. Bouchez, P. Paumard, et al., “Cell Energy Metabolism: An Update,” Biochimica et Biophysica (BBA) - Bioenergetics 1861, no. 11 (2020): 148276.

[23]

S. A. Mookerjee, A. A. Gerencser, D. G. Nicholls, and M. D. Brand, “Quantifying Intracellular Rates of Glycolytic and Oxidative ATP Production and Consumption Using Extracellular Flux Measurements,” Journal of Biological Chemistry 292, no. 17 (2017): 7189-7207.

[24]

P. J. Magistretti and I. Allaman, “Lactate in the Brain: From Metabolic End-product to Signalling Molecule,” Nature Reviews Neuroscience 19, no. 4 (2018): 235-249.

[25]

L. F. Barros, A. Brown, and R. A. Swanson, “Glia in Brain Energy Metabolism: A Perspective,” Glia 66, no. 6 (2018): 1134-1137.

[26]

K. Tao, N. Matsuki, and R. Koyama, “AMP-activated Protein Kinase Mediates Activity-dependent Axon Branching by Recruiting Mitochondria to Axon,” Developmental Neurobiology 74, no. 6 (2014): 557-573.

[27]

G. Ruthel and P. J. Hollenbeck, “Response of Mitochondrial Traffic to Axon Determination and Differential Branch Growth,” Journal of Neuroscience 23, no. 24 (2003): 8618-8624.

[28]

C. L. Zhang, P. L. Ho, D. B. Kintner, et al., “Activity-dependent Regulation of Mitochondrial Motility by Calcium and Na/K-ATPase at Nodes of Ranvier of Myelinated Nerves,” Journal of Neuroscience 30, no. 10 (2010): 3555-3566.

[29]

W. Dröge, “Free Radicals in the Physiological Control of Cell Function,” Physiological Reviews 82, no. 1 (2002): 47-95.

[30]

M. P. Murphy and R. C. Hartley, “Mitochondria as a Therapeutic Target for Common Pathologies,” Nat Rev Drug Discovery 17, no. 12 (2018): 865-886.

[31]

L. A. J. O'Neill, R. J. Kishton, and J. Rathmell, “A Guide to Immunometabolism for Immunologists,” Nature Reviews Immunology 16, no. 9 (2016): 553-565.

[32]

H. Tan, K. Yang, Y. Li, et al., “Integrative Proteomics and Phosphoproteomics Profiling Reveals Dynamic Signaling Networks and Bioenergetics Pathways Underlying T Cell Activation,” Immunity 46, no. 3 (2017): 488-503.

[33]

W. Y. Lam, A. M. Becker, K. M. Kennerly, et al., “Mitochondrial Pyruvate Import Promotes Long-Term Survival of Antibody-Secreting Plasma Cells,” Immunity 45, no. 1 (2016): 60-73.

[34]

E. Lachmandas, L. Boutens, J. M. Ratter, et al., “Microbial Stimulation of Different Toll-Like Receptor Signalling Pathways Induces Diverse Metabolic Programmes in human Monocytes,” Nature microbiology 2 (2016): 16246.

[35]

A. V. Kuznetsov, R. Margreiter, M. J. Ausserlechner, and J. Hagenbuchner, “The Complex Interplay Between Mitochondria, ROS and Entire Cellular Metabolism,” Antioxidants 11, no. 10 (2022): 1995.

[36]

Y. Liu, G. Fiskum, and D. Schubert, “Generation of Reactive Oxygen Species by the Mitochondrial Electron Transport Chain,” Journal of Neurochemistry 80, no. 5 (2002): 780-787.

[37]

Z. Zhao, “Iron and Oxidizing Species in Oxidative Stress and Alzheimer's Disease,” Aging Medicine Milton NSW 2, no. 2 (2019): 82-87.

[38]

A. Panov, “Perhydroxyl Radical (HO2•) as Inducer of the Isoprostane Lipid Peroxidation in Mitochondria,” Molecular Biology 52, no. 3 (2018): 295-305.

[39]

J. M. McCord and I. Fridovich, “Superoxide Dismutase. An Enzymic Function for Erythrocuprein (hemocuprein),” Journal of Biological Chemistry 244, no. 22 (1969): 6049-6055.

[40]

R. A. Weisiger and I. Fridovich, “Superoxide Dismutase. Organelle Specificity,” Journal of Biological Chemistry 248, no. 10 (1973): 3582-3592.

[41]

C. C. Winterbourn, “Toxicity of Iron and Hydrogen Peroxide: The Fenton Reaction,” Toxicology Letters 82-83 (1995): 969-974.

[42]

H. Sies and D. P. Jones, “Reactive Oxygen Species (ROS) as Pleiotropic Physiological Signalling Agents,” Nature Reviews Molecular Cell Biology 21, no. 7 (2020): 363-383.

[43]

S. G. Rhee, “Cell Signaling. H2O2, a Necessary Evil for Cell Signaling,” Science 312, no. 5782 (2006): 1882-1883.

[44]

M. Schieber and N. S. Chandel, “ROS Function in Redox Signaling and Oxidative Stress,” Current Biology 24, no. 10 (2014): R453-R462.

[45]

H. Sies, C. Berndt, and D. P. Jones, “Oxidative Stress,” Annual Review of Biochemistry 86 (2017): 715-748.

[46]

C. López-Otín, M. A. Blasco, L. Partridge, et al., “The Hallmarks of Aging,” Cell 153, no. 6 (2013): 1194-1217.

[47]

F. A. Court and M. P. Coleman, “Mitochondria as a central Sensor for Axonal Degenerative Stimuli,” Trends in Neuroscience (Tins) 35, no. 6 (2012): 364-372.

[48]

K. Biswas, K. Alexander, and M. M. Francis, “Reactive Oxygen Species: Angels and Demons in the Life of a Neuron,” NeuroScience 3, no. 1 (2022): 130-145.

[49]

L. A. Sena and N. S. Chandel, “Physiological Roles of Mitochondrial Reactive Oxygen Species,” Molecular Cell 48, no. 2 (2012): 158-167.

[50]

A. Hervera, F. De Virgiliis, I. Palmisano, et al., “Reactive Oxygen Species Regulate Axonal Regeneration Through the Release of Exosomal NADPH Oxidase 2 Complexes Into Injured Axons,” Nature Cell Biology 20, no. 3 (2018): 307-319.

[51]

M. C. Oswald, P. S. Brooks, M. F. Zwart, et al., “Reactive Oxygen Species Regulate Activity-dependent Neuronal Plasticity in Drosophila,” Elife 7 (2018): e39393.

[52]

A. W. K. Yeung, N. T. Tzvetkov, M. G. Georgieva, et al., “Reactive Oxygen Species and Their Impact in Neurodegenerative Diseases: Literature Landscape Analysis,” Antioxid Redox Signaling 34, no. 5 (2021): 402-420.

[53]

C. Wilson and C. González-Billault, “Regulation of Cytoskeletal Dynamics by Redox Signaling and Oxidative Stress: Implications for Neuronal Development and Trafficking,” Frontiers in Cellular Neuroscience 9 (2015): 381.

[54]

A. van der Pol, W. H. van Gilst, A. A. Voors, and P. van der Meer, “Treating Oxidative Stress in Heart Failure: Past, Present and Future,” European Journal of Heart Failure 21, no. 4 (2019): 425-435.

[55]

C. E. Pinzón-Díaz, J. V. Calderón-Salinas, M. M. Rosas-Flores, et al., “Eryptosis and Oxidative Damage in Hypertensive and Dyslipidemic Patients,” Molecular and Cellular Biochemistry 440, no. 1-2 (2018): 105-113.

[56]

M. A. Sánchez-Rodríguez and V. M. Mendoza-Núñez, “Oxidative Stress Indexes for Diagnosis of Health or Disease in Humans,” Oxidative Medicine and Cellular Longevity 2019, no. 1 (2019): 4128152.

[57]

A. Li, N. Zheng, and X. Ding, “Mitochondrial Abnormalities: A Hub in Metabolic Syndrome-related Cardiac Dysfunction Caused by Oxidative Stress,” Heart Failure Reviews 27, no. 4 (2022): 1387-1394.

[58]

H. Tirichen, H. Yaigoub, W. Xu, et al., “Mitochondrial Reactive Oxygen Species and Their Contribution in Chronic Kidney Disease Progression through Oxidative Stress,” Frontiers in Physiology 12 (2021): 627837.

[59]

Z. Geto, M. D. Molla, F. Challa, et al., “Mitochondrial Dynamic Dysfunction as a Main Triggering Factor for Inflammation Associated Chronic Non-Communicable Diseases,” Journal of Inflammation Research 13 (2020): 97-107.

[60]

V. Singh and S. Ubaid, “Role of Silent Information Regulator 1 (SIRT1) in Regulating Oxidative Stress and Inflammation,” Inflammation 43, no. 5 (2020): 1589-1598.

[61]

S. Pitkanen and B. H. Robinson, “Mitochondrial Complex I Deficiency Leads to Increased Production of Superoxide Radicals and Induction of Superoxide Dismutase,” Journal of Clinical Investigation 98, no. 2 (1996): 345-351.

[62]

H. M. Ni, J. A. Williams, and W. X. Ding, “Mitochondrial Dynamics and Mitochondrial Quality Control,” Redox Biology 4 (2015): 6-13.

[63]

M. Arai, H. Imai, T. Koumura, et al., “Mitochondrial Phospholipid Hydroperoxide Glutathione Peroxidase Plays a Major Role in Preventing Oxidative Injury to Cells,” Journal of Biological Chemistry 274, no. 8 (1999): 4924-4933.

[64]

R. Rizzuto, A. W. Simpson, M. Brini, and T. Pozzan, “Rapid Changes of Mitochondrial Ca2+ Revealed by Specifically Targeted Recombinant Aequorin,” Nature 358, no. 6384 (1992): 325-327.

[65]

E. D. Michelakis, “Mitochondrial Medicine: A New Era in Medicine Opens New Windows and Brings New Challenges,” Circulation 117, no. 19 (2008): 2431-2434.

[66]

M. Colombini, “The VDAC Channel: Molecular Basis for Selectivity,” Biochimica Et Biophysica Acta 1863, no. 10 (2016): 2498-2502.

[67]

D. De Stefani, A. Raffaello, E. Teardo, et al., “A Forty-kilodalton Protein of the Inner Membrane Is the Mitochondrial Calcium Uniporter,” Nature 476, no. 7360 (2011): 336-340.

[68]

J. M. Baughman, F. Perocchi, H. S. Girgis, et al., “Integrative Genomics Identifies MCU as an Essential Component of the Mitochondrial Calcium Uniporter,” Nature 476, no. 7360 (2011): 341-345.

[69]

O. Kann and R. Kovacs, “Mitochondria and Neuronal Activity,” American Journal of Physiology-Cell Physiology 292, no. 2 (2007): C641-C657.

[70]

D. Nicholls, “Mitochondria and Calcium Signaling,” Cell Calcium 38, no. 3-4 (2005): 311-317.

[71]

C. Picton, C. B. Klee, and P. Cohen, “The Regulation of Muscle Phosphorylase Kinase by Calcium Ions, Calmodulin and Troponin-C,” Cell Calcium 2, no. 4 (1981): 281-294.

[72]

J. G. McCormack, A. P. Halestrap, and R. M. Denton, “Role of Calcium Ions in Regulation of Mammalian Intramitochondrial Metabolism,” Physiological Reviews 70, no. 2 (1990): 391-425.

[73]

M. S. Müller, “Functional Impact of Glycogen Degradation on Astrocytic Signalling,” Biochemical Society Transactions 42, no. 5 (2014): 1311-1315.

[74]

L. S. Jouaville, P. Pinton, C. Bastianutto, et al., “Regulation of Mitochondrial ATP Synthesis by Calcium: Evidence for a Long-term Metabolic Priming,” PNAS 96, no. 24 (1999): 13807-13812.

[75]

R. Rizzuto, D. De Stefani, A. Raffaello, and C. Mammucari, “Mitochondria as Sensors and Regulators of Calcium Signalling,” Nature Reviews Molecular Cell Biology 13, no. 9 (2012): 566-578.

[76]

A. Herrero-Mendez, A. Almeida, E. Fernández, et al., “The Bioenergetic and Antioxidant Status of Neurons Is Controlled by Continuous Degradation of a Key Glycolytic Enzyme by APC/C-Cdh1,” Nature Cell Biology 11, no. 6 (2009): 747-752.

[77]

L. Tretter, K. Takacs, K. Kövér, and V. Adam-Vizi, “Stimulation of H(2)O(2) Generation by Calcium in Brain Mitochondria Respiring on Alpha-glycerophosphate,” Journal of Neuroscience Research 85, no. 15 (2007): 3471-3479.

[78]

C. Mammucari, A. Raffaello, D. Vecellio Reane, et al., “Mitochondrial Calcium Uptake in Organ Physiology: From Molecular Mechanism to Animal Models,” Pflugers Archiv: European journal of physiology 470, no. 8 (2018): 1165-1179.

[79]

D. Boehning, R. L. Patterson, L. Sedaghat, et al., “Cytochrome c Binds to Inositol (1,4,5) Trisphosphate Receptors, Amplifying Calcium-dependent Apoptosis,” Nature Cell Biology 5, no. 12 (2003): 1051-1061.

[80]

R. C. Reyes and V. Parpura, “Mitochondria Modulate Ca2+-dependent Glutamate Release From Rat Cortical Astrocytes,” The Journal of Neuroscience 28, no. 39 (2008): 9682-9691.

[81]

K. S. Lee, S. Huh, S. Lee, et al., “Altered ER-mitochondria Contact Impacts Mitochondria Calcium Homeostasis and Contributes to Neurodegeneration in Vivo in Disease Models,” PNAS 115, no. 38 (2018): E8844-E8853.

[82]

E. Zampese, C. Fasolato, T. Pozzan, and P. Pizzo, “Presenilin-2 Modulation of ER-mitochondria Interactions: FAD Mutations, Mechanisms and Pathological Consequences,” Communicative and Integrative Biology 4, no. 3 (2011): 357-360.

[83]

A. Rossi, G. Rigotto, G. Valente, et al., “Defective Mitochondrial Pyruvate Flux Affects Cell Bioenergetics in Alzheimer's Disease-Related Models,” Cell reports 30, no. 7 (2020): 2332-2348. e10.

[84]

D. J. Surmeier, P. T. Schumacker, J. D. Guzman, et al., “Calcium and Parkinson's Disease,” Biochemical and Biophysical Research Communications 483, no. 4 (2017): 1013-1019.

[85]

A. Agarwal, P. H. Wu, E. G. Hughes, et al., “Transient Opening of the Mitochondrial Permeability Transition Pore Induces Microdomain Calcium Transients in Astrocyte Processes,” Neuron 93, no. 3 (2017): 587-605. e7.

[86]

C. Giorgi, S. Marchi, and P. Pinton, “The Machineries, Regulation and Cellular Functions of Mitochondrial Calcium,” Nature Reviews Molecular Cell Biology 19, no. 11 (2018): 713-730.

[87]

M. Bonora, M. R. Wieckowski, D. A. Sinclair, et al., “Targeting Mitochondria for Cardiovascular Disorders: Therapeutic Potential and Obstacles,” Nature Reviews Cardiology 16, no. 1 (2019): 33-55.

[88]

A. Danese, S. Patergnani, M. Bonora, et al., “Calcium Regulates Cell Death in Cancer: Roles of the Mitochondria and Mitochondria-associated Membranes (MAMs),” Biochimica et Biophysica (BBA) - Bioenergetics 1858, no. 8 (2017): 615-627.

[89]

S. Patergnani, A. Danese, E. Bouhamida, et al., “Various Aspects of Calcium Signaling in the Regulation of Apoptosis, Autophagy, Cell Proliferation, and Cancer,” International Journal of Molecular Sciences 21, no. 21 (2020): 8323.

[90]

C. Cardanho-Ramos and V. A. Morais, “Mitochondrial Biogenesis in Neurons: How and Where,” International Journal of Molecular Sciences 22, no. 23 (2021): 13059.

[91]

R. C. Scarpulla, “Transcriptional Paradigms in Mammalian Mitochondrial Biogenesis and Function,” Physiological Reviews 88, no. 2 (2008): 611-638.

[92]

J. R. Friedman and J. Nunnari, “Mitochondrial Form and Function,” Nature 505, no. 7483 (2014): 335-343.

[93]

I. G. Onyango, J. Lu, M. Rodova, et al., “Regulation of Neuron Mitochondrial Biogenesis and Relevance to Brain Health,” Biochimica Et Biophysica Acta 1802, no. 1 (2010): 228-234.

[94]

M. Amiri and P. J. Hollenbeck, “Mitochondrial Biogenesis in the Axons of Vertebrate Peripheral Neurons,” Developmental Neurobiology 68, no. 11 (2008): 1348-1361.

[95]

A. Vaarmann, M. Mandel, A. Zeb, et al., “Mitochondrial Biogenesis Is Required for Axonal Growth,” Development (Cambridge, England) 143, no. 11 (2016): 1981-1992.

[96]

M. Golpich, E. Amini, Z. Mohamed, et al., “Mitochondrial Dysfunction and Biogenesis in Neurodegenerative Diseases: Pathogenesis and Treatment,” CNS Neuroscience & Therapeutics 23, no. 1 (2017): 5-22.

[97]

S. Jamwal, J. K. Blackburn, and J. D. Elsworth, “PPARγ/PGC1α Signaling as a Potential Therapeutic Target for Mitochondrial Biogenesis in Neurodegenerative Disorders,” Pharmacology & Therapeutics 219 (2021): 107705.

[98]

F. Ye and A. Wu, “The Protective Mechanism of SIRT1 in the Regulation of Mitochondrial Biogenesis and Mitochondrial Autophagy in Alzheimer's Disease,” Journal of Alzheimer's Disease 82, no. 1 (2021): 149-157.

[99]

S. A. Murphy, M. Miyamoto, A. Kervadec, et al., “PGC1/PPAR Drive Cardiomyocyte Maturation at Single Cell Level via YAP1 and SF3B2,” Nature Communications 12, no. 1 (2021): 1648.

[100]

H. Wang, W. J. Yan, J. L. Zhang, et al., “Adiponectin Partially Rescues High Glucose/High Fat-induced Impairment of Mitochondrial Biogenesis and Function in a PGC-1α Dependent Manner,” European Review for Medical and Pharmacological Sciences 21, no. 3 (2017): 590-599.

[101]

X. Zhang, Z. Zhang, Y. Zhao, et al., “Alogliptin, a Dipeptidyl Peptidase-4 Inhibitor, Alleviates Atrial Remodeling and Improves Mitochondrial Function and Biogenesis in Diabetic Rabbits,” Journal of the American Heart Association 6, no. 5 (2017): e005945.

[102]

G. A. Oriquat, M. A. Ali, S. A. Mahmoud, et al., “Improving Hepatic Mitochondrial Biogenesis as a Postulated Mechanism for the Antidiabetic Effect of Spirulina platensis in Comparison With metformin,” Applied Physiology, Nutrition, and Metabolism 44, no. 4 (2019): 357-364.

[103]

V. S. LeBleu, J. T. O'Connell, K. N. G. Herrera, et al., “PGC-1α Mediates Mitochondrial Biogenesis and Oxidative Phosphorylation to Promote Metastasis,” Nature Cell Biology 16, no. 10 (2014): 992-915.

[104]

A. De Luca, M. Fiorillo, M. Peiris-Pagès, et al., “Mitochondrial Biogenesis Is Required for the Anchorage-independent Survival and Propagation of Stem-Like Cancer Cells,” Oncotarget 6, no. 17 (2015): 14777-14795.

[105]

M. Gorska-Ponikowska, A. Kuban-Jankowska, S. A. Eisler, et al., “2-Methoxyestradiol Affects Mitochondrial Biogenesis Pathway and Succinate Dehydrogenase Complex Flavoprotein Subunit A in Osteosarcoma Cancer Cells,” Cancer Genomics & Proteomics 15, no. 1 (2018): 73-89.

[106]

T. Wai and T. Langer, “Mitochondrial Dynamics and Metabolic Regulation,” Trends in Endocrinology & Metabolism 27, no. 2 (2016): 105-117.

[107]

D. C. Chan, “Mitochondrial Dynamics and Its Involvement in Disease,” Annual Review of Pathology 15 (2020): 235-259.

[108]

K. R. Pitts, Y. Yoon, E. W. Krueger, and M. A. McNiven, “The Dynamin-Like Protein DLP1 Is Essential for Normal Distribution and Morphology of the Endoplasmic Reticulum and Mitochondria in Mammalian Cells,” Molecular Biology of the Cell 10, no. 12 (1999): 4403-4417.

[109]

E. Smirnova, L. Griparic, D. L. Shurland, and A. M. van der Bliek, “Dynamin-related Protein Drp1 Is Required for Mitochondrial Division in Mammalian Cells,” Molecular Biology of the Cell 12, no. 8 (2001): 2245-2256.

[110]

H. Otera, N. Miyata, O. Kuge, and K. Mihara, “Drp1-dependent Mitochondrial Fission via MiD49/51 Is Essential for Apoptotic Cristae Remodeling,” Journal of Cell Biology 212, no. 5 (2016): 531-544.

[111]

O. C. Losón, Z. Song, H. Chen, and D. C. Chan, “Fis1, Mff, MiD49, and MiD51 Mediate Drp1 Recruitment in Mitochondrial Fission,” Molecular Biology of the Cell 24, no. 5 (2013): 659-667.

[112]

F. Kraus, K. Roy, T. J. Pucadyil, and M. T. Ryan, “Function and Regulation of the Divisome for Mitochondrial Fission,” Nature 590, no. 7844 (2021): 57-66.

[113]

Z. Song, M. Ghochani, J. M. McCaffery, et al., “Mitofusins and OPA1 Mediate Sequential Steps in Mitochondrial Membrane Fusion,” Molecular Biology of the Cell 20, no. 15 (2009): 3525-3532.

[114]

A. S. Rambold, B. Kostelecky, and J. Lippincott-Schwartz, “Together We Are Stronger: Fusion Protects Mitochondria From Autophagosomal Degradation,” Autophagy 7, no. 12 (2011): 1568-1569.

[115]

N. Zemirli, E. Morel, and D. Molino, “Mitochondrial Dynamics in Basal and Stressful Conditions,” International Journal of Molecular Sciences 19, no. 2 (2018): 564.

[116]

M. Giacomello, A. Pyakurel, C. Glytsou, and L. Scorrano, “The Cell Biology of Mitochondrial Membrane Dynamics,” Nature Reviews Molecular Cell Biology 21, no. 4 (2020): 204-224.

[117]

D. Larrea, M. Pera, A. Gonnelli, et al., “MFN2 mutations in Charcot-Marie-Tooth Disease Alter Mitochondria-associated ER Membrane Function but Do Not Impair Bioenergetics,” Human Molecular Genetics 28, no. 11 (2019): 1782-1800.

[118]

A. B. Knott, G. Perkins, R. Schwarzenbacher, and E. Bossy-Wetzel, “Mitochondrial Fragmentation in Neurodegeneration,” Nature Reviews Neuroscience 9, no. 7 (2008): 505-518.

[119]

M. Liesa, M. Palacin, and A. Zorzano, “Mitochondrial Dynamics in Mammalian Health and Disease,” Physiological Reviews 89, no. 3 (2009): 799-845.

[120]

D. F. Kashatus, “The Regulation of Tumor Cell Physiology by Mitochondrial Dynamics,” Biochemical and Biophysical Research Communications 500, no. 1 (2018): 9-16.

[121]

J. Rehman, H. J. Zhang, P. T. Toth, et al., “Inhibition of Mitochondrial Fission Prevents Cell Cycle Progression in Lung Cancer,” The FASEB Journal 26, no. 5 (2012): 2175-2186.

[122]

J. A. Kashatus, A. Nascimento, L. J. Myers, et al., “Erk2 phosphorylation of Drp1 Promotes Mitochondrial Fission and MAPK-driven Tumor Growth,” Molecular Cell 57, no. 3 (2015): 537-551.

[123]

F. J. Bock and S. W. G. Tait, “Mitochondria as Multifaceted Regulators of Cell Death,” Nature Reviews Molecular Cell Biology 21, no. 2 (2020): 85-100.

[124]

J. Song, J. M. Herrmann, and T. Becker, “Quality Control of the Mitochondrial Proteome,” Nature Reviews Molecular Cell Biology 22, no. 1 (2021): 54-70.

[125]

A. Sugiura, G. L. McLelland, E. A. Fon, and H. M. McBride, “A New Pathway for Mitochondrial Quality Control: Mitochondrial-derived Vesicles,” Embo Journal 33, no. 19 (2014): 2142-2156.

[126]

T. König, H. Nolte, M. J. Aaltonen, et al., “MIROs and DRP1 Drive Mitochondrial-derived Vesicle Biogenesis and Promote Quality Control,” Nature Cell Biology 23, no. 12 (2021): 1271-1286.

[127]

A. Picca, J. Faitg, J. Auwerx, et al., “Mitophagy in human Health, Ageing and Disease,” Nature Metabolism 5, no. 12 (2023): 2047-2061.

[128]

A. C. Poole, R. E. Thomas, L. A. Andrews, et al., “The PINK1/Parkin Pathway Regulates Mitochondrial Morphology,” PNAS 105, no. 5 (2008): 1638-1643.

[129]

I. E. Clark, M. W. Dodson, C. Jiang, et al., “Drosophila pink1 Is Required for Mitochondrial Function and Interacts Genetically With Parkin,” Nature 441, no. 7097 (2006): 1162-1166.

[130]

E. M. Valente, P. M. Abou-Sleiman, V. Caputo, et al., “Hereditary Early-onset Parkinson's Disease Caused by Mutations in PINK1,” Science 304, no. 5674 (2004): 1158-1160.

[131]

T. Kitada, S. Asakawa, N. Hattori, et al., “Mutations in the Parkin Gene Cause Autosomal Recessive Juvenile Parkinsonism,” Nature 392, no. 6676 (1998): 605-608.

[132]

S. A. Sarraf, M. Raman, V. Guarani-Pereira, et al., “Landscape of the PARKIN-dependent Ubiquitylome in Response to Mitochondrial Depolarization,” Nature 496, no. 7445 (2013): 372-376.

[133]

M. Lazarou, D. A. Sliter, L. A. Kane, et al., “The Ubiquitin Kinase PINK1 Recruits Autophagy Receptors to Induce Mitophagy,” Nature 524, no. 7565 (2015): 309-314.

[134]

M. Y. W. Ng, T. Wai, and A. Simonsen, “Quality Control of the Mitochondrion,” Developmental Cell 56, no. 7 (2021): 881-905.

[135]

T. T. Ho, M. R. Warr, E. R. Adelman, et al., “Autophagy Maintains the Metabolism and Function of Young and Old Stem Cells,” Nature 543, no. 7644 (2017): 205-210.

[136]

M. N. Quinsay, R. L. Thomas, Y. Lee, and A. B. Gustafsson, “Bnip3-mediated Mitochondrial Autophagy Is Independent of the Mitochondrial Permeability Transition Pore,” Autophagy 6, no. 7 (2010): 855-862.

[137]

H. Shitara, H. Kaneda, A. Sato, et al., “Selective and Continuous Elimination of Mitochondria Microinjected Into Mouse Eggs From Spermatids, but Not From Liver Cells, Occurs throughout Embryogenesis,” Genetics 156, no. 3 (2000): 1277-1284.

[138]

S. M. Jin and R. J. Youle, “PINK1- and Parkin-mediated Mitophagy at a Glance,” Journal of Cell Science 125, no. Pt 4 (2012): 795-799.

[139]

E. F. Fang, Y. Hou, K. Palikaras, et al., “Mitophagy Inhibits Amyloid-β and Tau Pathology and Reverses Cognitive Deficits in Models of Alzheimer's Disease,” Nature Neuroscience 22, no. 3 (2019): 401-412.

[140]

S. Hwang, M. H. Disatnik, and D. Mochly-Rosen, “Impaired GAPDH-induced Mitophagy Contributes to the Pathology of Huntington's Disease,” EMBO Molecular Medicine 7, no. 10 (2015): 1307-1326.

[141]

J. P. Bernardini, M. Lazarou, and G. Dewson, “Parkin and Mitophagy in Cancer,” Oncogene 36, no. 10 (2017): 1315-1327.

[142]

S. Ito, J. Araya, Y. Kurita, et al., “PARK2-mediated Mitophagy Is Involved in Regulation of HBEC Senescence in COPD Pathogenesis,” Autophagy 11, no. 3 (2015): 547-559.

[143]

H. Bugger and K. Pfeil, “Mitochondrial ROS in Myocardial Ischemia Reperfusion and Remodeling,” Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1866, no. 7 (2020): 165768.

[144]

H. Pei, Y. Yang, H. Zhao, et al., “The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases,” Oxidative Medicine and Cellular Longevity 2016 (2016): 5470457.

[145]

L. Galluzzi, J. M. Bravo-San Pedro, I. Vitale, et al., “Essential versus Accessory Aspects of Cell Death: Recommendations of the NCCD 2015,” Cell Death and Differentiation 22, no. 1 (2015): 58-73.

[146]

F. H. Igney and P. H. Krammer, “Death and Anti-death: Tumour Resistance to Apoptosis,” Nature Reviews Cancer 2, no. 4 (2002): 277-288.

[147]

S. Elmore, “Apoptosis: A Review of Programmed Cell Death,” Toxicologic Pathology 35, no. 4 (2007): 495-516.

[148]

D. R. Green and G. Kroemer, “The Pathophysiology of Mitochondrial Cell Death,” Science 305, no. 5684 (2004): 626-629.

[149]

H. L. Vieira and G. Kroemer, “Pathophysiology of Mitochondrial Cell Death Control,” Cellular and Molecular Life Sciences CMLS 56, no. 11-12 (1999): 971-976.

[150]

R. J. Youle and A. Strasser, “The BCL-2 Protein family: Opposing Activities That Mediate Cell Death,” Nature Reviews Molecular Cell Biology 9, no. 1 (2008): 47-59.

[151]

C. Hockings, K. Anwari, R. L. Ninnis, et al., “Bid Chimeras Indicate That Most BH3-only Proteins Can Directly Activate Bak and Bax, and Show no Preference for Bak versus Bax,” Cell Death & Disease 6, no. 4 (2015): e1735.

[152]

H. Zou, W. J. Henzel, X. Liu, et al., “Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c-Dependent Activation of Caspase-3,” Cell 90, no. 3 (1997): 405-413.

[153]

P. Li, D. Nijhawan, I. Budihardjo, et al., “Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade,” Cell 91, no. 4 (1997): 479-489.

[154]

X. Liu, C. N. Kim, J. Yang, et al., “Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c,” Cell 86, no. 1 (1996): 147-157.

[155]

K. N. Alavian, G. Beutner, E. Lazrove, et al., “An Uncoupling Channel Within the c-subunit Ring of the F1FO ATP Synthase Is the Mitochondrial Permeability Transition Pore,” Pnas 111, no. 29 (2014): 10580-10585.

[156]

V. Giorgio, S. Von Stockum, M. Antoniel, et al., “Dimers of Mitochondrial ATP Synthase Form the Permeability Transition Pore,” Pnas 110, no. 15 (2013): 5887-5892.

[157]

N. Mnatsakanyan and E. A. Jonas, “The New Role of F1Fo ATP Synthase in Mitochondria-mediated Neurodegeneration and Neuroprotection,” Experimental Neurology 332 (2020): 113400.

[158]

S. Orrenius, V. Gogvadze, and B. Zhivotovsky, “Calcium and Mitochondria in the Regulation of Cell Death,” Biochemical and Biophysical Research Communications 460, no. 1 (2015): 72-81.

[159]

C. P. Baines, R. A. Kaiser, N. H. Purcell, et al., “Loss of Cyclophilin D Reveals a Critical Role for Mitochondrial Permeability Transition in Cell Death,” Nature 434, no. 7033 (2005): 658-662.

[160]

B. Fadeel and S. Orrenius, “Apoptosis: A Basic Biological Phenomenon With Wide-ranging Implications in human Disease,” Journal of Internal Medicine 258, no. 6 (2005): 479-517.

[161]

N. Salvadores, M. Sanhueza, P. Manque, and F. A. Court, “Axonal Degeneration During Aging and Its Functional Role in Neurodegenerative Disorders,” Frontiers in Neuroscience 11 (2017): 451.

[162]

S. Saxena and P. Caroni, “Mechanisms of Axon Degeneration: From Development to Disease,” Progress in Neurobiology 83, no. 3 (2007): 174-191.

[163]

T. G. Cotter, “Apoptosis and Cancer: The Genesis of a Research Field,” Nature Reviews Cancer 9, no. 7 (2009): 501-507.

[164]

N. S. Erekat, “Apoptosis and Its Therapeutic Implications in Neurodegenerative Diseases,” Clinical Anatomy 35, no. 1 (2022): 65-78.

[165]

A. Roulston, R. C. Marcellus, and P. E. Branton, “Viruses and Apoptosis,” Annual Review of Microbiology 53 (1999): 577-628.

[166]

N. W. Cummins and A. D. Badley, “Mechanisms of HIV-associated Lymphocyte Apoptosis: 2010,” Cell Death & Disease 1, no. 11 (2010): e99.

[167]

G. Olivetti, F. Quaini, R. Sala, et al., “Acute Myocardial Infarction in Humans Is Associated With Activation of Programmed Myocyte Cell Death in the Surviving Portion of the Heart,” Journal of Molecular and Cellular Cardiology 28, no. 9 (1996): 2005-2016.

[168]

A. Saraste, K. Pulkki, M. Kallajoki, et al., “Apoptosis in human Acute Myocardial Infarction,” Circulation 95, no. 2 (1997): 320-323.

[169]

A. Abbate, G. G. L. Biondi-Zoccai, R. Bussani, et al., “Increased Myocardial Apoptosis in Patients With Unfavorable Left Ventricular Remodeling and Early Symptomatic Post-infarction Heart Failure,” Journal of the American College of Cardiology 41, no. 5 (2003): 753-760.

[170]

J. L. Gollihue and A. G. Rabchevsky, “Prospects for Therapeutic Mitochondrial Transplantation,” Mitochondrion 35 (2017): 70-79.

[171]

J. D. McCully, D. B. Cowan, S. M. Emani, and P. J. Del Nido, “Mitochondrial Transplantation: From Animal Models to Clinical Use in Humans,” Mitochondrion 34 (2017): 127-134.

[172]

C. C. Kuo, H. L. Su, T. L. Chang, et al., “Prevention of Axonal Degeneration by Perineurium Injection of Mitochondria in a Sciatic Nerve Crush Injury Model,” Neurosurgery 80, no. 3 (2017): 475-488.

[173]

K. Liu, L. Guo, Z. Zhou, et al., “Mesenchymal Stem Cells Transfer Mitochondria Into Cerebral Microvasculature and Promote Recovery From Ischemic Stroke,” Microvascular Research 123 (2019): 74-80.

[174]

M. N. Islam, S. R. Das, M. T. Emin, et al., “Mitochondrial Transfer From Bone Marrow-derived Stromal Cells to Pulmonary Alveoli Protects Against Acute Lung Injury,” Nature Medicine 18, no. 5 (2012): 759-765.

[175]

X. Shi, M. Zhao, C. Fu, and A. Fu, “Intravenous Administration of Mitochondria for Treating Experimental Parkinson's Disease,” Mitochondrion 34 (2017): 91-100.

[176]

M. Vos, E. Lauwers, and P. Verstreken, “Synaptic Mitochondria in Synaptic Transmission and Organization of Vesicle Pools in Health and Disease,” Frontiers in Synaptic Neuroscience 2 (2010): 139.

[177]

Y. Wang, J. Ni, C. Gao, et al., “Mitochondrial Transplantation Attenuates Lipopolysaccharide- induced Depression-Like Behaviors,” Progress in Neuro-Psychopharmacology & Biological Psychiatry 93 (2019): 240-249.

[178]

K. Hayakawa, E. Esposito, X. Wang, et al., “Transfer of Mitochondria From Astrocytes to Neurons After Stroke,” Nature 535, no. 7613 (2016): 551-555.

[179]

Y. C. Chuang, C. W. Liou, S. D. Chen, et al., “Mitochondrial Transfer From Wharton's Jelly Mesenchymal Stem Cell to MERRF Cybrid Reduces Oxidative Stress and Improves Mitochondrial Bioenergetics,” Oxidative Medicine and Cellular Longevity 2017 (2017): 5691215.

[180]

J. Zhao, D. Qu, Z. Xi, et al., “Mitochondria Transplantation Protects Traumatic Brain Injury via Promoting Neuronal Survival and Astrocytic BDNF,” Translational Research Journal of Laboratory and Clinical Medicine 235 (2021): 102-114.

[181]

Z. Zhang, Z. Ma, C. Yan, et al., “Muscle-derived Autologous Mitochondrial Transplantation: A Novel Strategy for Treating Cerebral Ischemic Injury,” Behavioural Brain Research 356 (2019): 322-331.

[182]

Z. Zhao, Y. Hou, W. Zhou, et al., “Mitochondrial Transplantation Therapy Inhibit Carbon Tetrachloride-induced Liver Injury Through Scavenging Free Radicals and Protecting Hepatocytes,” Bioengineering & Translational Medicine 6, no. 2 (2021): e10209.

[183]

L. Xia, C. Zhang, N. Lv, et al., “AdMSC-derived Exosomes Alleviate Acute Lung Injury via Transferring Mitochondrial Component to Improve Homeostasis of Alveolar Macrophages,” Theranostics 12, no. 6 (2022): 2928-2947.

[184]

Y. Guo, X. Chi, Y. Wang, et al., “Mitochondria Transfer Enhances Proliferation, Migration, and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cell and Promotes Bone Defect Healing,” Stem Cell Research and Therapy 11 (2020): 245.

[185]

C. Cornelius, R. Crupi, V. Calabrese, et al., “Traumatic Brain Injury: Oxidative Stress and Neuroprotection,” Antioxid Redox Signaling 19, no. 8 (2013): 836-853.

[186]

P. J. Huang, C. C. Kuo, H. C. Lee, et al., “Transferring Xenogenic Mitochondria Provides Neural Protection against Ischemic Stress in Ischemic Rat Brains,” Cell Transplantation 25, no. 5 (2016): 913-927.

[187]

M. W. Lin, S. Y. Fang, J. Y. C. Hsu, et al., “Mitochondrial Transplantation Attenuates Neural Damage and Improves Locomotor Function after Traumatic Spinal Cord Injury in Rats,” Frontiers in neuroscience 16 (2022): 800883.

[188]

N. Konari, K. Nagaishi, S. Kikuchi, and M. Fujimiya, “Mitochondria Transfer From Mesenchymal Stem Cells Structurally and Functionally Repairs Renal Proximal Tubular Epithelial Cells in Diabetic Nephropathy in Vivo,” Scientific Reports 9 (2019): 5184.

[189]

C. T. Madreiter-Sokolowski, C. Thomas, and M. Ristow, “Interrelation Between ROS and Ca2+ in Aging and Age-related Diseases,” Redox Biology 36 (2020): 101678.

[190]

E. Cadenas and A. Boveris, “Enhancement of Hydrogen Peroxide Formation by Protophores and Ionophores in Antimycin-supplemented Mitochondria,” Biochemical Journal 188, no. 1 (1980): 31-37.

[191]

A. Görlach, K. Bertram, S. Hudecova, and O. Krizanova, “Calcium and ROS: A Mutual Interplay,” Redox Biology 6 (2015): 260-271.

[192]

Z. Liu, Y. Sun, Z. Qi, et al., “Mitochondrial Transfer/Transplantation: An Emerging Therapeutic Approach for Multiple Diseases,” Cell BioSciences 12, no. 1 (2022): 66.

[193]

B. Mokhtari, R. Yavari, R. Badalzadeh, and A. Mahmoodpoor, “An Overview on Mitochondrial-Based Therapies in Sepsis-Related Myocardial Dysfunction: Mitochondrial Transplantation as a Promising Approach,” Canadian Journal of Infectious Diseases and Medical Microbiology 2022 (2022): 3277274.

[194]

S. D. Skaper, L. Facci, M. Zusso, and P. Giusti, “An Inflammation-Centric View of Neurological Disease: Beyond the Neuron,” Frontiers in Cellular Neuroscience 12 (2018): 72.

[195]

S. Y. Fang, J. N. Roan, J. S. Lee, et al., “Transplantation of Viable Mitochondria Attenuates Neurologic Injury After Spinal Cord Ischemia,” Journal of Thoracic and Cardiovascular Surgery 161, no. 5 (2021): e337-e347.

[196]

C. C. Huang, H. Y. Chiu, P. H. Lee, et al., “Mitochondrial Transplantation Attenuates Traumatic Neuropathic Pain, Neuroinflammation, and Apoptosis in Rats With Nerve Root Ligation,” Molecular Pain 19 (2023): 17448069231210423.

[197]

B. Zhang, C. Pan, C. Feng, et al., “Role of Mitochondrial Reactive Oxygen Species in Homeostasis Regulation,” Redox Report: Communications in Free Radical Research 27, no. 1 (2022): 45-52.

[198]

U. Kaur, P. Banerjee, A. Bir, et al., “Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection,” Current Topics in Medicinal Chemistry 15, no. 5 (2015): 446-457.

[199]

D. S. A. Simpson and P. L. Oliver, “ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease,” Antioxidants 9, no. 8 (2020): 743.

[200]

Y. Yuan, L. Yuan, L. Li, et al., “Mitochondrial Transfer From Mesenchymal Stem Cells to Macrophages Restricts Inflammation and Alleviates Kidney Injury in Diabetic Nephropathy Mice via PGC-1α Activation,” Stem Cells (Dayton, Ohio) 39, no. 7 (2021): 913-928.

[201]

S. H. Yu, S. Kim, Y. Kim, et al., “Human Umbilical Cord Mesenchymal Stem Cell-derived Mitochondria (PN-101) Attenuate LPS-induced Inflammatory Responses by Inhibiting NFκB Signaling Pathway,” BMB Reports 55, no. 3 (2022): 136-141.

[202]

C. Yan, Z. Ma, H. Ma, et al., “Mitochondrial Transplantation Attenuates Brain Dysfunction in Sepsis by Driving Microglial M2 Polarization,” Molecular Neurobiology 57, no. 9 (2020): 3875-3890.

[203]

X. Jia, Q. Wang, J. Ji, et al., “Mitochondrial Transplantation Ameliorates Hippocampal Damage Following Status Epilepticus,” Animal Models and Experimental Medicine 6, no. 1 (2023): 41-50.

[204]

C. Bamshad, M. Habibi Roudkenar, M. Abedinzade, et al., “Human Umbilical Cord-derived Mesenchymal Stem Cells-harvested Mitochondrial Transplantation Improved Motor Function in TBI Models Through Rescuing Neuronal Cells From Apoptosis and Alleviating Astrogliosis and Microglia Activation,” International Immunopharmacology 118 (2023): 110106.

[205]

L. Galluzzi, O. Kepp, C. Trojel-Hansen, and G. Kroemer, “Mitochondrial Control of Cellular Life, Stress, and Death,” Circulation Research 111, no. 9 (2012): 1198-1207.

[206]

G. Kroemer and J. C. Reed, “Mitochondrial Control of Cell Death,” Nature Medicine 6, no. 5 (2000): 513-519.

[207]

D. R. Green and J. C. Reed, “Mitochondria and Apoptosis,” Science 281, no. 5381 (1998): 1309-1312.

[208]

P. Norat, S. Soldozy, J. D. Sokolowski, et al., “Mitochondrial Dysfunction in Neurological Disorders: Exploring Mitochondrial Transplantation,” NPJ Regenerative Medicine 5, no. 1 (2020): 22.

[209]

A. Park, M. Oh, S. J. Lee, et al., “Mitochondrial Transplantation as a Novel Therapeutic Strategy for Mitochondrial Diseases,” International Journal of Molecular Sciences 22, no. 9 (2021): 4793.

[210]

J. C. Chang, S. L. Wu, K. H. Liu, et al., “Allogeneic/Xenogeneic Transplantation of Peptide-labeled Mitochondria in Parkinson's disease: Restoration of Mitochondria Functions and Attenuation of 6-hydroxydopamine-induced Neurotoxicity,” Translational Research Journal of Laboratory and Clinical Medicine 170 (2016): 40-56. e3.

[211]

H. W. Hyatt and S. K. Powers, “Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting due to Disease, Aging, and Prolonged Inactivity,” Antioxidants 10, no. 4 (2021): 588.

[212]

C. Shi, H. Guo, and X. Liu, “Platelet Mitochondria Transplantation Rescues Hypoxia/Reoxygenation-Induced Mitochondrial Dysfunction and Neuronal Cell Death Involving the FUNDC2/PIP3/Akt/FOXO3a Axis,” Cell Transplantation 30 (2021): 9636897211024210.

[213]

Q. Xie, J. Zeng, Y. Zheng, et al., “Mitochondrial Transplantation Attenuates Cerebral Ischemia-Reperfusion Injury: Possible Involvement of Mitochondrial Component Separation,” Oxidative Medicine and Cellular Longevity 2021 (2021): 1006636.

[214]

J. D. Ly, D. R. Grubb, and A. Lawen, “The Mitochondrial Membrane Potential (deltapsi(m)) in Apoptosis; an Update,” Apoptosis: A Review of Programmed Cell Death 8, no. 2 (2003): 115-128.

[215]

L. Hosseini, M. Karimipour, F. Seyedaghamiri, et al., “Intranasal Administration of Mitochondria Alleviated Cognitive Impairments and Mitochondrial Dysfunction in the Photothrombotic Model of mPFC Stroke in Mice,” Journal of Stroke and Cerebrovascular Diseases Off Journal National Stroke Association 31, no. 12 (2022): 106801.

[216]

O. Robicsek, H. M. Ene, R. Karry, et al., “Isolated Mitochondria Transfer Improves Neuronal Differentiation of Schizophrenia-Derived Induced Pluripotent Stem Cells and Rescues Deficits in a Rat Model of the Disorder,” Schizophrenia Bulletin 44, no. 2 (2018): 432-442.

[217]

V. Weixler, R. Lapusca, G. Grangl, et al., “Autogenous Mitochondria Transplantation for Treatment of Right Heart Failure,” Journal of Thoracic and Cardiovascular Surgery 162, no. 1 (2021): e111-e121.

[218]

A. Masuzawa, K. M. Black, C. A. Pacak, et al., “Transplantation of Autologously Derived Mitochondria Protects the Heart From Ischemia-reperfusion Injury,” American Journal of Physiology-Heart and Circulatory Physiology 304, no. 7 (2013): H966-H982.

[219]

H. Jabbari, A. M. Roushandeh, M. K. Rostami, et al., “Mitochondrial Transplantation Ameliorates Ischemia/Reperfusion-induced Kidney Injury in Rat,” Biochimica et Biophysica Acta - Molecular Basis of Disease 1866, no. 8 (2020): 165809.

[220]

J. W. Hwang, M. J. Lee, T. N. Chung, et al., “The Immune Modulatory Effects of Mitochondrial Transplantation on Cecal Slurry Model in Rat,” Critical Care (London, England) 25, no. 1 (2021): 20.

[221]

F. Zhang, X. Zheng, F. Zhao, et al., “TFAM-Mediated Mitochondrial Transfer of MSCs Improved the Permeability Barrier in Sepsis-associated Acute Lung Injury,” Apoptosis: An International Journal on Programmed Cell Death 28, no. 7-8 (2023): 1048-1059.

[222]

G. B. Kubat, M. Ozler, O. Ulger, et al., “The Effects of Mesenchymal Stem Cell Mitochondrial Transplantation on Doxorubicin-mediated Nephrotoxicity in Rats,” Journal of Biochemical and Molecular Toxicology 35, no. 1 (2021): e22612.

[223]

M. J. Kim, J. M. Lee, K. Min, and Y. S. Choi, “Xenogeneic Transplantation of Mitochondria Induces Muscle Regeneration in an in Vivo Rat Model of Dexamethasone-induced Atrophy,” Journal of Muscle Research and Cell Motility 45, no. 2 (2024): 53-68.

[224]

S. E. Alway, H. G. Paez, C. R. Pitzer, et al., “Xenogeneic Transplantation of Mitochondria Induces Muscle Regeneration in an in Vivo,” Journal of Cachexia, Sarcopenia and Muscle 14, no. 1 (2023): 493-507.

[225]

J. Suh, N. K. Kim, W. Shim, et al., “Mitochondrial Fragmentation and Donut Formation Enhance Mitochondrial Secretion to Promote Osteogenesis,” Cell metabolism 35, no. 2 (2023): 345-360. e7.

[226]

C. Y. Chang, M. Z. Liang, and L. Chen, “Current Progress of Mitochondrial Transplantation That Promotes Neuronal Regeneration,” Translational Neurodegeneration 8 (2019): 17.

[227]

L. Chien, M. Z. Liang, C. Y. Chang, et al., “Mitochondrial Therapy Promotes Regeneration of Injured Hippocampal Neurons,” Biochimica et Biophysica Acta - Molecular Basis of Disease 1864, no. 9 Pt B (2018): 3001-3012.

[228]

G. Nascimento-Dos-Santos, E. de-Souza-Ferreira, R. Lani, et al., “Neuroprotection From Optic Nerve Injury and Modulation of Oxidative Metabolism by Transplantation of Active Mitochondria to the Retina,” Biochimica et Biophysica Acta - Molecular Basis of Disease 1866, no. 5 (2020): 165686.

[229]

G. M. Smith and G. Gallo, “The Role of Mitochondria in Axon Development and Regeneration,” Developmental Neurobiology 78, no. 3 (2018): 221-237.

[230]

T. Chen, Y. Zhu, J. Jia, et al., “Mitochondrial Transplantation Promotes Remyelination and Long-Term Locomotion Recovery Following Cerebral Ischemia,” Mediators of Inflammation 2022 (2022): 1346343.

[231]

J. L. Gollihue, S. P. Patel, and A. G. Rabchevsky, “Mitochondrial Transplantation Strategies as Potential Therapeutics for central Nervous System Trauma,” Neural Regeneration Research 13, no. 2 (2018): 194-197.

[232]

C. Schiliro and B. L. Firestein, “Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation,” Cells 10, no. 5 (2021): 1056.

[233]

J. Ježek, K. F. Cooper, and R. Strich, “Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression,” Antioxidants 7, no. 1 (2018): 13.

[234]

J. L. Spees, S. D. Olson, M. J. Whitney, and D. J. Prockop, “Mitochondrial Transfer Between Cells Can Rescue Aerobic Respiration,” PNAS 103, no. 5 (2006): 1283-1288.

[235]

C. Sun, X. Liu, B. Wang, et al., “Endocytosis-mediated Mitochondrial Transplantation: Transferring Normal human Astrocytic Mitochondria Into Glioma Cells Rescues Aerobic Respiration and Enhances Radiosensitivity,” Theranostics 9, no. 12 (2019): 3595-3607.

[236]

J. C. Chang, H. S. Chang, Y. C. Wu, et al., “Mitochondrial Transplantation Regulates Antitumour Activity, Chemoresistance and Mitochondrial Dynamics in Breast Cancer,” Journal of Experimental & Clinical Cancer Research 38 (2019): 30.

[237]

Z. Yu, Y. Hou, W. Zhou, et al., “The Effect of Mitochondrial Transplantation Therapy From Different Gender on Inhibiting Cell Proliferation of Malignant Melanoma,” International Journal of Biological Sciences 17, no. 8 (2021): 2021-2033.

[238]

R. L. Elliott, X. P. Jiang, and J. F. Head, “Mitochondria Organelle Transplantation: Introduction of Normal Epithelial Mitochondria Into human Cancer Cells Inhibits Proliferation and Increases Drug Sensitivity,” Breast Cancer Research and Treatment 136, no. 2 (2012): 347-354.

[239]

W. Zhou, Z. Zhao, Z. Yu, et al., “Mitochondrial Transplantation Therapy Inhibits the Proliferation of Malignant Hepatocellular Carcinoma and Its Mechanism,” Mitochondrion 65 (2022): 11-22.

[240]

V. Aggarwal, H. S. Tuli, A. Varol, et al., “Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements,” Biomolecules 9, no. 11 (2019): 735.

[241]

A. Cruz-Gregorio, A. K. Aranda-Rivera, J. Pedraza-Chaverri, et al., “Redox-sensitive Signaling Pathways in Renal Cell Carcinoma,” BioFactors (Oxford, England) 48, no. 2 (2022): 342-358.

[242]

E. C. Cheung, G. M. DeNicola, C. Nixon, et al., “Dynamic ROS Control by TIGAR Regulates the Initiation and Progression of Pancreatic Cancer,” Cancer Cell 37, no. 2 (2020): 168-182. e4.

[243]

C. Wiel, K. Le Gal, M. X. Ibrahim, et al., “BACH1 Stabilization by Antioxidants Stimulates Lung Cancer Metastasis,” Cell 178, no. 2 (2019): 330-345. e22.

[244]

E. Piskounova, M. Agathocleous, M. M. Murphy, et al., “Oxidative Stress Inhibits Distant Metastasis by human Melanoma Cells,” Nature 527, no. 7577 (2015): 186-191.

[245]

L. F. Abbott and S. B. Nelson, “Synaptic Plasticity: Taming the Beast,” Nature Neuroscience 3, no. 11 (2000): 1178-1183.

[246]

A. Citri and R. C. Malenka, “Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms,” Neuropsychopharmacol Off Publ Am Coll Neuropsychopharmacol 33, no. 1 (2008): 18-41.

[247]

A. S. Dashkova, V. I. Kovalev, A. V. Chaplygina, et al., “Unique Properties of Synaptosomes and Prospects for Their Use for the Treatment of Alzheimer's Disease,” Biochemistry (Moscow) 89, no. 6 (2024): 1031-1044.

[248]

A. Faria-Pereira and V. A. Morais, “Synapses: The Brain's Energy-Demanding Sites,” International Journal of Molecular Sciences 23, no. 7 (2022): 3627.

[249]

Z. Li, K. I. Okamoto, Y. Hayashi, and M. Sheng, “The Importance of Dendritic Mitochondria in the Morphogenesis and Plasticity of Spines and Synapses,” Cell 119, no. 6 (2004): 873-887.

[250]

M. A. Sutton and E. M. Schuman, “Dendritic Protein Synthesis, Synaptic Plasticity, and Memory,” Cell 127, no. 1 (2006): 49-58.

[251]

Z. H. Sheng and Q. Cai, “Mitochondrial Transport in Neurons: Impact on Synaptic Homeostasis and Neurodegeneration,” Nature Reviews Neuroscience 13, no. 2 (2012): 77-93.

[252]

B. Zhang, Y. Gao, Q. Li, et al., “Effects of Brain-Derived Mitochondria on the Function of Neuron and Vascular Endothelial Cell after Traumatic Brain Injury,” World neurosurgery 138 (2020): e1-e9.

[253]

C. Severini, “Neurotrophic Factors in Health and Disease,” Cells 12, no. 1 (2022): 47.

[254]

E. E. Benarroch, “Brain-derived Neurotrophic Factor: Regulation, Effects, and Potential Clinical Relevance,” Neurology 84, no. 16 (2015): 1693-1704.

[255]

F. Zheng, Y. Luo, and H. Wang, “Regulation of BDNF-mediated Transcription of Immediate Early Gene Arc by Intracellular Calcium and Calmodulin,” Journal of Neuroscience Research 87, no. 2 (2009): 380-392.

[256]

A. J. Kowaltowski, S. L. Menezes-Filho, E. A. Assali, et al., “Mitochondrial Morphology Regulates Organellar Ca2+ Uptake and Changes Cellular Ca2+ Homeostasis,” FASEB J Off Publ Fed Am Soc Exp Biol 33, no. 12 (2019): 13176-13188.

[257]

L. Luo, “Architectures of Neuronal Circuits,” Science 373, no. 6559 (2021): eabg7285.

[258]

H. Eo, S. H. Yu, Y. Choi, et al., “Mitochondrial Transplantation Exhibits Neuroprotective Effects and Improves Behavioral Deficits in an Animal Model of Parkinson's Disease,” Neurotherapeutics: The journal of the American Society for Experimental NeuroTherapeutics 21, no. 4 (2024): e00355.

[259]

F. Bradke, J. W. Fawcett, and M. E. Spira, “Assembly of a New Growth Cone After Axotomy: The Precursor to Axon Regeneration,” Nature Reviews Neuroscience 13, no. 3 (2012): 183-193.

[260]

B. Yang, F. Zhang, F. Cheng, et al., “Strategies and Prospects of Effective Neural Circuits Reconstruction After Spinal Cord Injury,” Cell Death & Disease 11, no. 6 (2020): 1-14.

[261]

A. Oyarzabal and I. Marin-Valencia, “Synaptic Energy Metabolism and Neuronal Excitability, in Sickness and Health,” Journal of Inherited Metabolic Disease 42, no. 2 (2019): 220-236.

[262]

B. Lu, G. Nagappan, and Y. Lu, “BDNF and Synaptic Plasticity, Cognitive Function, and Dysfunction,” Handbook of Experimental Pharmacology 220 (2014): 223-250.

[263]

S. S. Kang, M. P. Keasey, S. A. Arnold, et al., “Endogenous CNTF Mediates Stroke-induced Adult CNS Neurogenesis in Mice,” Neurobiology of Disease 49 (2013): 68-78.

[264]

Y. Xiao and T. Czopka, “Myelination-independent Functions of Oligodendrocyte Precursor Cells in Health and Disease,” Nature Neuroscience 26, no. 10 (2023): 1663-1669.

[265]

A. Lopez Juarez, D. He, and Q. Richard Lu, “Oligodendrocyte Progenitor Programming and Reprogramming: Toward Myelin Regeneration,” Brain Research 1638 (2016): 209-220.

[266]

A. M. Bertholet, T. Delerue, A. M. Millet, et al., “Mitochondrial Fusion/Fission Dynamics in Neurodegeneration and Neuronal Plasticity,” Neurobiology of Disease 90 (2016): 3-19.

[267]

M. A. Clark and J. W. Shay, “Mitochondrial Transformation of Mammalian Cells,” Nature 295, no. 5850 (1982): 605-607.

[268]

J. D. McCully, D. B. Cowan, C. A. Pacak, et al., “Injection of Isolated Mitochondria During Early Reperfusion for Cardioprotection,” American Journal of Physiology-Heart and Circulatory Physiology 296, no. 1 (2009): H94-H105.

[269]

K. Tripathi and D. Ben-Shachar, “Mitochondria in the Central Nervous System in Health and Disease: The Puzzle of the Therapeutic Potential of Mitochondrial Transplantation,” Cells 13, no. 5 (2024): 410.

[270]

J. Suh and Y. S. Lee, “Mitochondria as Secretory Organelles and Therapeutic Cargos,” Experimental & Molecular Medicine 56, no. 1 (2024): 66-85.

[271]

N. Borcherding and J. R. Brestoff, “The Power and Potential of Mitochondria Transfer,” Nature 623, no. 7986 (2023): 283-291.

[272]

Y. Nakamura, J. H. Park, and K. Hayakawa, “Therapeutic Use of Extracellular Mitochondria in CNS Injury and Disease,” Experimental Neurology 324 (2020): 113114.

[273]

F. Liu, J. Lu, A. Manaenko, J. Tang, and Q. Hu, “Mitochondria in Ischemic Stroke: New Insight and Implications,” Aging and Disease 9, no. 5 (2018): 924-937.

[274]

C. Li, M. K. H. Cheung, S. Han, et al., “Mesenchymal Stem Cells and Their Mitochondrial Transfer: A Double-edged Sword,” Bioscience Reports 39, no. 5 (2019): BSR20182417.

[275]

D. Liu, Y. Gao, J. Liu, et al., “Intercellular Mitochondrial Transfer as a Means of Tissue Revitalization,” Signal Transduction and Targeted Therapy 6, no. 1 (2021): 65.

[276]

S. Paliwal, R. Chaudhuri, A. Agrawal, and S. Mohanty, “Regenerative Abilities of Mesenchymal Stem Cells Through Mitochondrial Transfer,” Journal of Biomedical Science 25 (2018): 31.

[277]

J. C. Chang, Y. C. Chao, H. S. Chang, et al., “Intranasal Delivery of Mitochondria for Treatment of Parkinson's Disease Model Rats Lesioned With 6-hydroxydopamine,” Scientific Reports 11, no. 1 (2021): 10597.

[278]

K. Nitzan, S. Benhamron, M. Valitsky, et al., “Mitochondrial Transfer Ameliorates Cognitive Deficits, Neuronal Loss, and Gliosis in Alzheimer's Disease Mice,” Journal of Alzheimer's Disease 72, no. 2 (2019): 587-604.

[279]

S. Sweetat, K. Nitzan, N. Suissa, et al., “The Beneficial Effect of Mitochondrial Transfer Therapy in 5XFAD Mice via Liver-Serum-Brain Response,” Cells 12, no. 7 (2023): 1006.

[280]

Z. Zhang, D. Wei, Z. Li, et al., “Hippocampal Mitochondrial Transplantation Alleviates Age-Associated Cognitive Decline via Enhancing Wnt Signaling and Neurogenesis,” Computational Intelligence and Neuroscience 2022 (2022): 9325302.

[281]

H. Ma, T. Jiang, W. Tang, et al., “Transplantation of Platelet-derived Mitochondria Alleviates Cognitive Impairment and Mitochondrial Dysfunction in db/db Mice,” Clinical Science (London, England: 1979) 134, no. 16 (2020): 2161-2175.

[282]

G. Javani, S. Babri, F. Farajdokht, et al., “Mitochondrial Transplantation Improves Anxiety- and Depression-Like Behaviors in Aged Stress-exposed Rats,” Mechanisms of Ageing and Development 202 (2022): 111632.

[283]

Z. Zhao, Z. Yu, Y. Hou, et al., “Improvement of Cognitive and Motor Performance With Mitotherapy in Aged Mice,” International Journal of Biological Sciences 16, no. 5 (2020): 849-858.

[284]

J. L. Gollihue, S. P. Patel, K. C. Eldahan, et al., “Effects of Mitochondrial Transplantation on Bioenergetics, Cellular Incorporation, and Functional Recovery After Spinal Cord Injury,” Journal of Neurotrauma 35, no. 15 (2018): 1800-1818.

[285]

Z. Pourmohammadi-Bejarpasi, A. M. Roushandeh, A. Saberi, et al., “Mesenchymal Stem Cells-derived Mitochondria Transplantation Mitigates I/R-induced Injury, Abolishes I/R-induced Apoptosis, and Restores Motor Function in Acute Ischemia Stroke Rat Model,” Brain Research Bulletin 165 (2020): 70-80.

[286]

Y. Nakamura, E. H. Lo, and K. Hayakawa, “Placental Mitochondria Therapy for Cerebral Ischemia-Reperfusion Injury in Mice,” Stroke; A Journal of Cerebral Circulation 51, no. 10 (2020): 3142-3146.

[287]

H. Li, C. Wang, T. He, et al., “Mitochondrial Transfer From Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction,” Theranostics 9, no. 7 (2019): 2017-2035.

[288]

V. A. Babenko, D. N. Silachev, L. D. Zorova, et al., “Improving the Post-Stroke Therapeutic Potency of Mesenchymal Multipotent Stromal Cells by Cocultivation with Cortical Neurons: The Role of Crosstalk between Cells,” Stem Cells Translational Medicine 4, no. 9 (2015): 1011-1020.

[289]

H. K. Yip, N. K. Dubey, K. C. Lin, et al., “Melatonin Rescues Cerebral Ischemic Events Through Upregulated Tunneling Nanotube-mediated Mitochondrial Transfer and Downregulated Mitochondrial Oxidative Stress in Rat Brain,” Biomedicine & Pharmacotherapy 139 (2021): 111593.

[290]

N. V. Bobkova, D. Y. Zhdanova, N. V. Belosludtseva, et al., “Intranasal Administration of Mitochondria Improves Spatial Memory in Olfactory Bulbectomized Mice,” Experimental Biology and Medicine 247, no. 5 (2022): 416-425.

[291]

J. F. Alexander, A. V. Seua, L. D. Arroyo, et al., “Nasal Administration of Mitochondria Reverses Chemotherapy-induced Cognitive Deficits,” Theranostics 11, no. 7 (2021): 3109-3130.

[292]

N. Boukelmoune, G. S. Chiu, A. Kavelaars, and C. J. Heijnen, “Mitochondrial Transfer From Mesenchymal Stem Cells to Neural Stem Cells Protects Against the Neurotoxic Effects of Cisplatin,” Acta Neuropathologica Communications 6, no. 1 (2018): 139.

[293]

L. Peruzzotti-Jametti, J. D. Bernstock, C. M. Willis, et al., “Neural Stem Cells Traffic Functional Mitochondria via Extracellular Vesicles,” Plos Biology 19, no. 4 (2021): e3001166.

[294]

K. M. Dave, D. B. Stolz, V. R. Venna, et al., “Mitochondria-containing Extracellular Vesicles (EV) Reduce Mouse Brain Infarct Sizes and EV/HSP27 Protect Ischemic Brain Endothelial Cultures,” J Control Release Off J Control Release Soc 354 (2023): 368-393.

[295]

D. B. Cowan, R. Yao, V. Akurathi, et al., “Intracoronary Delivery of Mitochondria to the Ischemic Heart for Cardioprotection,” PLoS ONE 11, no. 8 (2016): e0160889.

[296]

A. K. Kaza, I. Wamala, I. Friehs, et al., “Myocardial Rescue With Autologous Mitochondrial Transplantation in a Porcine Model of Ischemia/Reperfusion,” Journal of Thoracic and Cardiovascular Surgery 153, no. 4 (2017): 934-943.

[297]

B. Shin, M. Y. Saeed, J. J. Esch, et al., “A Novel Biological Strategy for Myocardial Protection by Intracoronary Delivery of Mitochondria: Safety and Efficacy,” JACC Basic Transl Sci 4, no. 8 (2019): 871-888.

[298]

G. Alvise, P. D. Ilias, D. Thomas, et al., “Mitochondrial Transplantation for Myocardial Protection in Ex-situ‒Perfused Hearts Donated After Circulatory Death,” J Heart Lung Transplant Off Publ Int Soc Heart Transplant 39, no. 11 (2020): 1279-1288.

[299]

D. Blitzer, A. Guariento, I. P. Doulamis, et al., “Delayed Transplantation of Autologous Mitochondria for Cardioprotection in a Porcine Model,” Annals of Thoracic Surgery 109, no. 3 (2020): 711-719.

[300]

K. Moskowitzova, B. Shin, K. Liu, et al., “Mitochondrial Transplantation Prolongs Cold Ischemia Time in Murine Heart Transplantation,” J Heart Lung Transplant Off Publ Int Soc Heart Transplant 38, no. 1 (2019): 92-99.

[301]

I. P. Doulamis, A. Guariento, T. Duignan, et al., “Mitochondrial Transplantation for Myocardial Protection in Diabetic Hearts,” Eur J Cardio-Thorac Surg Off J Eur Assoc Cardio-Thorac Surg 57, no. 5 (2020): 836-845.

[302]

Y. Zhang, Z. Yu, D. Jiang, et al., “iPSC-MSCs With High Intrinsic MIRO1 and Sensitivity to TNF-α Yield Efficacious Mitochondrial Transfer to Rescue Anthracycline-Induced Cardiomyopathy,” Stem Cell Reports 7, no. 4 (2016): 749-763.

[303]

G. Ikeda, M. R. Santoso, Y. Tada, et al., “Mitochondria-Rich Extracellular Vesicles From Autologous Stem Cell-Derived Cardiomyocytes Restore Energetics of Ischemic Myocardium,” Journal of the American College of Cardiology 77, no. 8 (2021): 1073-1088.

[304]

X. Shi, H. Bai, M. Zhao, et al., “Treatment of Acetaminophen-induced Liver Injury With Exogenous Mitochondria in Mice,” Transl Res J Lab Clin Med 196 (2018): 31-41.

[305]

O. Ulger, G. B. Kubat, Z. Cicek, et al., “The Effects of Mitochondrial Transplantation in Acetaminophen-induced Liver Toxicity in Rats,” Life Sciences 279 (2021): 119669.

[306]

A. Fu, X. Shi, H. Zhang, and B. Fu, “Mitotherapy for Fatty Liver by Intravenous Administration of Exogenous Mitochondria in Male Mice,” Frontiers in pharmacology 8 (2017): 241.

[307]

H. C. Lin, S. Y. Liu, H. S. Lai, and I. R. Lai, “Isolated Mitochondria Infusion Mitigates Ischemia-reperfusion Injury of the Liver in Rats,” Shock Augusta Ga 39, no. 3 (2013): 304-310.

[308]

T. Lu, J. Zhang, J. Cai, et al., “Extracellular Vesicles Derived From Mesenchymal Stromal Cells as Nanotherapeutics for Liver Ischaemia-reperfusion Injury by Transferring Mitochondria to Modulate the Formation of Neutrophil Extracellular Traps,” Biomaterials 284 (2022): 121486.

[309]

C. M. Cloer, C. S. Givens, L. K. Buie, et al., “Mitochondrial Transplant After Ischemia Reperfusion Promotes Cellular Salvage and Improves Lung Function During Ex-vivo Lung Perfusion,” J Heart Lung Transplant Off Publ Int Soc Heart Transplant 42, no. 5 (2023): 575-584.

[310]

K. Moskowitzova, A. Orfany, K. Liu, et al., “Mitochondrial Transplantation Enhances Murine Lung Viability and Recovery After Ischemia-reperfusion Injury,” Am J Physiol—Lung Cell Mol Physiol 318, no. 1 (2020): L78-L88.

[311]

T. Huang, T. Zhang, X. Jiang, et al., “Iron Oxide Nanoparticles Augment the Intercellular Mitochondrial Transfer-mediated Therapy,” Science Advances 7, no. 40 (2021): eabj0534.

[312]

A. Rossi, A. Asthana, C. Riganti, et al., “Mitochondria Transplantation Mitigates Damage in an in Vitro Model of Renal Tubular Injury and in an Ex Vivo Model of DCD Renal Transplantation,” Annals of Surgery 278, no. 6 (2023): e1313-e1326.

[313]

I. P. Doulamis, A. Guariento, T. Duignan, et al., “Mitochondrial Transplantation by Intra-arterial Injection for Acute Kidney Injury,” American Journal of Physiology. Renal Physiology 319, no. 3 (2020): F403-F413.

[314]

M. Zhao, S. Liu, C. Wang, et al., “Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Mitochondrial Damage and Inflammation by Stabilizing Mitochondrial DNA,” ACS Nano 15, no. 1 (2021): 1519-1538.

[315]

H. Cao, Y. Cheng, H. Gao, et al., “In Vivo Tracking of Mesenchymal Stem Cell-Derived Extracellular Vesicles Improving Mitochondrial Function in Renal Ischemia-Reperfusion Injury,” ACS Nano 14, no. 4 (2020): 4014-4026.

[316]

J. M. Lee, J. W. Hwang, M. J. Kim, et al., “Mitochondrial Transplantation Modulates Inflammation and Apoptosis, Alleviating Tendinopathy both in Vivo and in Vitro,” Antioxid Basel Switz 10, no. 5 (2021): 696.

[317]

A. Orfany, C. G. Arriola, I. P. Doulamis, et al., “Mitochondrial Transplantation Ameliorates Acute Limb Ischemia,” Journal of Vascular Surgery 71, no. 3 (2020): 1014-1026.

[318]

J. Sun, H. T. J. Lo, L. Fan, et al., “High-efficiency Quantitative Control of Mitochondrial Transfer Based on Droplet Microfluidics and Its Application on Muscle Regeneration,” Science Advances 8, no. 33 (2022): eabp9245.

[319]

A. R. Lee, J. S. Woo, S. Y. Lee, et al., “Mitochondrial Transplantation Ameliorates the Development and Progression of Osteoarthritis,” Immune Netw 22, no. 2 (2022): e14.

[320]

Z. Zhang, C. Yan, J. Miao, et al., “Muscle-Derived Mitochondrial Transplantation Reduces Inflammation, Enhances Bacterial Clearance, and Improves Survival in Sepsis,” Shock Augusta Ga 56, no. 1 (2021): 108-118.

[321]

L. R. P. de Carvalho, S. C. Abreu, L. L. de Castro, et al., “Mitochondria-Rich Fraction Isolated from Mesenchymal Stromal Cells Reduces Lung and Distal Organ Injury in Experimental Sepsis,” Critical Care Medicine 49, no. 9 (2021): e880-e890.

[322]

Y. S. Kim, H. A. R. Lee, M. J. Lee, et al., “The Effects of Mitochondrial Transplantation on Sepsis Depend on the Type of Cell From Which They Are Isolated,” International Journal of Molecular Sciences 24, no. 12 (2023): 10113.

[323]

A. C. Court, A. Le-Gatt, P. Luz-Crawford, et al., “Mitochondrial Transfer From MSCs to T Cells Induces Treg Differentiation and Restricts Inflammatory Response,” Embo Reports 21, no. 2 (2020): e48052.

[324]

J. C. Chang, H. S. Chang, Y. C. Wu, et al., “Antitumor Actions of Intratumoral Delivery of Membrane-Fused Mitochondria in a Mouse Model of Triple-Negative Breast Cancers,” OncoTargets Ther 13 (2020): 5241-5255.

[325]

J. C. Chang, H. S. Chang, C. Y. Yeh, et al., “Regulation of Mitochondrial Fusion and Mitophagy by Intra-tumoral Delivery of Membrane-fused Mitochondria or Midiv-1 Enhances Sensitivity to Doxorubicin in Triple-negative Breast Cancer,” Biomedicine & Pharmacotherapy 153 (2022): 113484.

[326]

A. Fu, Y. Hou, Z. Yu, et al., “Healthy Mitochondria Inhibit the Metastatic Melanoma in Lungs,” Int J Biol Sci 15, no. 12 (2019): 2707-2718.

[327]

C. A. Pinkert, M. H. Irwin, L. W. Johnson, and R. J. Moffatt, “Mitochondria Transfer Into Mouse Ova by Microinjection,” Transgenic Research 6, no. 6 (1997): 379-383.

[328]

A. Caicedo, V. Fritz, J. M. Brondello, et al., “MitoCeption as a New Tool to Assess the Effects of Mesenchymal Stem/Stromal Cell Mitochondria on Cancer Cell Metabolism and Function,” Scientific Reports 5 (2015): 9073.

[329]

F. Cabrera, M. Ortega, F. Velarde, et al., “Primary Allogeneic Mitochondrial Mix (PAMM) Transfer/Transplant by MitoCeption to Address Damage in PBMCs Caused by Ultraviolet Radiation,” BMC Biotechnology [Electronic Resource] 19, no. 1 (2019): 42.

[330]

T. Macheiner, V. H. I. Fengler, M. Agreiter, et al., “Magnetomitotransfer: An Efficient Way for Direct Mitochondria Transfer Into Cultured human Cells,” Scientific Reports 6 (2016): 35571.

[331]

J. C. Chang, K. H. Liu, Y. C. Li, et al., “Functional Recovery of human Cells Harbouring the Mitochondrial DNA Mutation MERRF A8344G via Peptide-mediated Mitochondrial Delivery,” Neuro-Signals 21, no. 3-4 (2013): 160-173.

[332]

S. Wu, A. Zhang, S. Li, et al., “Polymer Functionalization of Isolated Mitochondria for Cellular Transplantation and Metabolic Phenotype Alteration,” Adv Sci Weinh Baden-Wurtt Ger 5, no. 3 (2018): 1700530.

[333]

T. H. Wu, E. Sagullo, D. Case, et al., “Mitochondrial Transfer by Photothermal Nanoblade Restores Metabolite Profile in Mammalian Cells,” Cell metabolism 23, no. 5 (2016): 921-929.

[334]

A. J. Sercel, A. N. Patananan, T. Man, et al., “Stable Transplantation of human Mitochondrial DNA by High-throughput, Pressurized Isolated Mitochondrial Delivery,” Elife 10 (2021): e63102.

[335]

T. H. Wu, Y. C. Wu, E. Sagullo, et al., “Direct Nuclear Delivery of DNA by Photothermal Nanoblade,” J Lab Autom 20, no. 6 (2015): 659-662.

[336]

C. G. Gäbelein, Q. Feng, E. Sarajlic, et al., “Mitochondria Transplantation Between Living Cells,” Plos Biology 20, no. 3 (2022): e3001576.

[337]

P. Picone, G. Porcelli, C. C. Bavisotto, et al., “Synaptosomes: New Vesicles for Neuronal Mitochondrial Transplantation,” J Nanobiotechnology 19 (2021): 6.

[338]

N. Tseng, S. C. Lambie, C. Q. Huynh, et al., “Mitochondrial Transfer From Mesenchymal Stem Cells Improves Neuronal Metabolism After Oxidant Injury in Vitro: The Role of Miro1,” J Cereb Blood Flow Metab Off J Int Soc Cereb Blood Flow Metab 41, no. 4 (2021): 761-770.

[339]

X. Li, Y. Li, Z. Zhang, et al., “Mild Hypothermia Facilitates Mitochondrial Transfer From Astrocytes to Injured Neurons During Oxygen-glucose Deprivation/Reoxygenation,” Neuroscience Letters 756 (2021): 135940.

[340]

X. Y. Cheng, S. Biswas, J. Li, et al., “Human iPSCs Derived Astrocytes Rescue Rotenone-induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Vitro by Donating Functional Mitochondria,” Transl Neurodegener 9, no. 1 (2020): 13.

[341]

K. English, A. Shepherd, N. E. Uzor, et al., “Astrocytes Rescue Neuronal Health After Cisplatin Treatment Through Mitochondrial Transfer,” Acta Neuropathol Commun 8, no. 1 (2020): 36.

[342]

M. Mahrouf-Yorgov, L. Augeul, C. C. Da Silva, et al., “Mesenchymal Stem Cells Sense Mitochondria Released From Damaged Cells as Danger Signals to Activate Their Rescue Properties,” Cell Death and Differentiation 24, no. 7 (2017): 1224-1238.

[343]

H. Han, J. Hu, Q. Yan, et al., “Bone Marrow-derived Mesenchymal Stem Cells Rescue Injured H9c2 Cells via Transferring Intact Mitochondria Through Tunneling Nanotubes in an in Vitro Simulated Ischemia/Reperfusion Model,” Mol Med Rep 13, no. 2 (2016): 1517-1524.

[344]

S. Kim, Y. Kim, S. H. Yu, et al., “Platelet-derived Mitochondria Transfer Facilitates Wound-closure by Modulating ROS Levels in Dermal Fibroblasts,” Platelets 34, no. 1 (2022): 2151996.

[345]

P. Jin, Q. Pan, Y. Lin, et al., “Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells,” Oxid Med Cell Longev 2023 (2023): 2345279.

[346]

K. Unuma, T. Aki, T. Funakoshi, et al., “Extrusion of Mitochondrial Contents From Lipopolysaccharide-stimulated Cells: Involvement of Autophagy,” Autophagy 11, no. 9 (2015): 1520-1536.

[347]

A. Arjmand, S. Shiranirad, F. Ameritorzani, et al., “Mitochondrial Transplantation Against Gentamicin-induced Toxicity on Rat Renal Proximal Tubular Cells: The Higher Activity of Female Rat Mitochondria,” In Vitro Cellular & Developmental Biology Animal 59, no. 1 (2023): 31-40.

[348]

E. Seydi, M. Rahemi, H. Esmaily, et al., “Mitochondrial Transplantation Attenuates Toxicity in Rat Renal Proximal Tubular Cells Caused by Favipiravir,” Journal of Pharmacy and Pharmacology 75, no. 11 (2023): 1458-1466.

[349]

A. Arjmand, M. Faizi, M. Rezaei, and J. Pourahmad, “The Effect of Donor Rat Gender in Mitochondrial Transplantation Therapy of Cisplatin-Induced Toxicity on Rat Renal Proximal Tubular Cells,” Iran J Pharm Res IJPR 22, no. 1 (2023): e135666.

[350]

M. J. Kim, J. W. Hwang, C. K. Yun, et al., “Delivery of Exogenous Mitochondria via Centrifugation Enhances Cellular Metabolic Function,” Scientific Reports 8, no. 1 (2018): 3330.

[351]

V. Budnik, C. Ruiz-Cañada, and F. Wendler, “Extracellular Vesicles Round off Communication in the Nervous System,” Nature Reviews Neuroscience 17, no. 3 (2016): 160-172.

[352]

S. Ahmad, R. K. Srivastava, P. Singh, et al., “Role of Extracellular Vesicles in Glia-Neuron Intercellular Communication,” Frontiers in Molecular Neuroscience 15 (2022): 844194.

[353]

S. M. Emani, B. L. Piekarski, D. Harrild, et al., “Autologous Mitochondrial Transplantation for Dysfunction After Ischemia-reperfusion Injury,” Journal of Thoracic and Cardiovascular Surgery 154, no. 1 (2017): 286-289.

[354]

A. Yoshimi, K. Ishikawa, C. Niemeyer, and S. C. Grünert, “Pearson Syndrome: A Multisystem Mitochondrial Disease With Bone Marrow Failure,” Orphanet journal of rare diseases 17, no. 1 (2022): 379.

[355]

A. Guariento, B. L. Piekarski, I. P. Doulamis, et al., “Autologous Mitochondrial Transplantation for Cardiogenic Shock in Pediatric Patients Following Ischemia-reperfusion Injury,” Journal of Thoracic and Cardiovascular Surgery 162, no. 3 (2021): 992-1001.

[356]

M. Walker, E. Federico, Y. Sancak, and M. R. Levitt, “Mitochondrial Transplantation in Ischemic Stroke: Insights From a First-in-Human Brain Trial,” Current Transplantation Reports 11, no. 2 (2024): 53-62.

[357]

M. Sun, W. Jiang, N. Mu, et al., “Mitochondrial Transplantation as a Novel Therapeutic Strategy for Cardiovascular Diseases,” Journal of translational medicine 21 (2023): 347.

[358]

R. Jain, N. Begum, K. P. Tryphena, et al., “Inter and Intracellular Mitochondrial Transfer: Future of Mitochondrial Transplant Therapy in Parkinson's Disease,” Biomedicine & Pharmacotherapy 159 (2023): 114268.

[359]

C. E. D. la Fuente-Muñoz and C. Arias, “The Therapeutic Potential of Mitochondrial Transplantation for the Treatment of Neurodegenerative Disorders,” Reviews in the Neurosciences 32, no. 2 (2021): 203-217.

[360]

Y. Chen, F. Yang, Y. Chu, et al., “Mitochondrial Transplantation: Opportunities and Challenges in the Treatment of Obesity, Diabetes, and Nonalcoholic Fatty Liver Disease,” Journal of translational medicine 20, no. 1 (2022): 1-16.

[361]

A. Cruz-Gregorio, A. K. Aranda-Rivera, I. Amador-Martinez, and P. Maycotte, “Mitochondrial Transplantation Strategies in Multifaceted Induction of Cancer Cell Death,” Life Sciences 332 (2023): 122098.

[362]

E. M. Fock and R. G. Parnova, “Protective Effect of Mitochondria-Targeted Antioxidants Against Inflammatory Response to Lipopolysaccharide Challenge: A Review,” Pharmaceutics 13, no. 2 (2021): 144.

[363]

A. C. Bulua, A. Simon, R. Maddipati, et al., “Mitochondrial Reactive Oxygen Species Promote Production of Proinflammatory Cytokines and Are Elevated in TNFR1-associated Periodic Syndrome (TRAPS),” Journal of Experimental Medicine 208, no. 3 (2011): 519-533.

[364]

A. Rimessi, M. Previati, F. Nigro, et al., “Mitochondrial Reactive Oxygen Species and Inflammation: Molecular Mechanisms, Diseases and Promising Therapies,” International Journal of Biochemistry & Cell Biology 81 (2016): 281-293.

[365]

J. R. Mercer, E. Yu, N. Figg, et al., “The Mitochondria-targeted Antioxidant MitoQ Decreases Features of the Metabolic Syndrome in ATM+/-/ApoE-/- mice,” Free Radical Biology and Medicine 52, no. 5 (2012): 841-849.

[366]

R. Ni, T. Cao, S. Xiong, et al., “Therapeutic Inhibition of Mitochondrial Reactive Oxygen Species With mito-TEMPO Reduces Diabetic Cardiomyopathy,” Free Radical Biology and Medicine 90 (2016): 12-23.

[367]

J. McLachlan, E. Beattie, M. P. Murphy, et al., “Combined Therapeutic Benefit of Mitochondria-targeted Antioxidant, MitoQ10, and Angiotensin Receptor Blocker, Losartan, on Cardiovascular Function,” Journal of Hypertension 32, no. 3 (2014): 555-564.

[368]

D. Graham, N. N. Huynh, C. A. Hamilton, et al., “Mitochondria-targeted Antioxidant MitoQ10 Improves Endothelial Function and Attenuates Cardiac Hypertrophy,” Hypertens Dallas Tex 1979 54, no. 2 (2009): 322-328.

[369]

T. A. Ajith, “Role of Mitochondria and Mitochondria-targeted Agents in Non-alcoholic Fatty Liver Disease,” Clinical and Experimental Pharmacology & Physiology 45, no. 5 (2018): 413-421.

[370]

K. Gariani, K. J. Menzies, D. Ryu, et al., “Eliciting the Mitochondrial Unfolded Protein Response by Nicotinamide Adenine Dinucleotide Repletion Reverses Fatty Liver Disease in Mice,” Hepatol Baltim Md 63, no. 4 (2016): 1190-1204.

[371]

S. A. Mortensen, F. Rosenfeldt, A. Kumar, et al., “The Effect of Coenzyme Q10 on Morbidity and Mortality in Chronic Heart Failure: Results From Q-SYMBIO: A Randomized Double-blind Trial,” JACC Heart Fail 2, no. 6 (2014): 641-649.

[372]

F. Forini, P. Canale, G. Nicolini, and G. Iervasi, “Mitochondria-Targeted Drug Delivery in Cardiovascular Disease: A Long Road to Nano-Cardio Medicine,” Pharmaceutics 12, no. 11 (2020): 1122.

[373]

X. Du, Q. Zeng, Y. Luo, et al., “Application Research of Novel Peptide Mitochondrial-targeted Antioxidant SS-31 in Mitigating Mitochondrial Dysfunction,” Mitochondrion 75 (2024): 101846.

[374]

E. Miquel, A. Cassina, L. Martínez-Palma, et al., “Neuroprotective Effects of the Mitochondria-targeted Antioxidant MitoQ in a Model of Inherited Amyotrophic Lateral Sclerosis,” Free Radical Biology and Medicine 70 (2014): 204-213.

[375]

H. Komaki, N. Faraji, A. Komaki, et al., “Investigation of Protective Effects of Coenzyme Q10 on Impaired Synaptic Plasticity in a Male Rat Model of Alzheimer's Disease,” Brain Research Bulletin 147 (2019): 14-21.

[376]

P. J. Flannery and E. Trushina, “Mitochondrial Dysfunction in Alzheimer's Disease and Progress in Mitochondria-Targeted Therapeutics,” Current Behavioral Neuroscience Reports 6, no. 3 (2019): 88-102.

[377]

S. Bido, F. N. Soria, R. Z. Fan, E. Bezard, and K. Tieu, “Mitochondrial Division Inhibitor-1 Is Neuroprotective in the A53T-α-synuclein Rat Model of Parkinson's disease,” Scientific Reports 7, no. 1 (2017): 7495.

[378]

S. H. Baek, S. J. Park, J. I. Jeong, et al., “Inhibition of Drp1 Ameliorates Synaptic Depression, Aβ Deposition, and Cognitive Impairment in an Alzheimer's Disease Model,” The Journal of Neuroscience 37, no. 20 (2017): 5099-5110.

[379]

Y. Zhao, X. Sun, D. Hu, et al., “ATAD3A oligomerization Causes Neurodegeneration by Coupling Mitochondrial Fragmentation and Bioenergetics Defects,” Nature Communications 10, no. 1 (2019): 1371.

[380]

L. Zhang, S. Zhang, I. Maezawa, et al., “Modulation of Mitochondrial Complex I Activity Averts Cognitive Decline in Multiple Animal Models of Familial Alzheimer's Disease,” EBioMedicine 2, no. 4 (2015): 294-305.

[381]

W. Zhao, M. Varghese, P. Vempati, et al., “Caprylic Triglyceride as a Novel Therapeutic Approach to Effectively Improve the Performance and Attenuate the Symptoms due to the Motor Neuron Loss in ALS Disease,” PLoS ONE 7, no. 11 (2012): e49191.

[382]

T. W. Tefera, Y. Wong, M. E. Barkl-Luke, et al., “Triheptanoin Protects Motor Neurons and Delays the Onset of Motor Symptoms in a Mouse Model of Amyotrophic Lateral Sclerosis,” PLoS ONE 11, no. 8 (2016): e0161816.

[383]

D. A. Butterfield and B. Halliwell, “Oxidative Stress, Dysfunctional Glucose Metabolism and Alzheimer Disease,” Nature Reviews Neuroscience 20, no. 3 (2019): 148-160.

[384]

K. Tieu, C. Perier, C. Caspersen, et al., “D-beta-hydroxybutyrate Rescues Mitochondrial Respiration and Mitigates Features of Parkinson disease,” Journal of Clinical Investigation 112, no. 6 (2003): 892-901.

[385]

Z. Ou, X. Kong, X. Sun, et al., “Metformin Treatment Prevents Amyloid Plaque Deposition and Memory Impairment in APP/PS1 Mice,” Brain, Behavior, and Immunity 69 (2018): 351-363.

[386]

I. Arnoux, M. Willam, N. Griesche, et al., “Metformin Reverses Early Cortical Network Dysfunction and Behavior Changes in Huntington's disease,” Elife 7 (2018): e38744.

[387]

H. H. Szeto and A. V. Birk, “Serendipity and the Discovery of Novel Compounds That Restore Mitochondrial Plasticity,” Clinical Pharmacology & Therapeutics 96, no. 6 (2014): 672-683.

[388]

V. J. A. Jameson, H. M. Cochemé, A. Logan, et al., “Synthesis of Triphenylphosphonium Vitamin E Derivatives as Mitochondria-targeted Antioxidants,” Tetrahedron 71, no. 44 (2015): 8444-8453.

[389]

T. Khan, R. Waseem, Z. Zehra, et al., “Mitochondrial Dysfunction: Pathophysiology and Mitochondria-Targeted Drug Delivery Approaches,” Pharmaceutics 14, no. 12 (2022): 2657.

[390]

M. Picard, T. Taivassalo, D. Ritchie, et al., “Mitochondrial Structure and Function Are Disrupted by Standard Isolation Methods,” PLoS ONE 6, no. 3 (2011): e18317.

[391]

I. R. Lanza and K. S. Nair, “Functional Assessment of Isolated Mitochondria in Vitro,” Methods in Enzymology 457 (2009): 349-372.

[392]

A. P. West and G. S. Shadel, “Mitochondrial DNA in Innate Immune Responses and Inflammatory Pathology,” Nature Reviews Immunology 17, no. 6 (2017): 363-375.

[393]

A. P. West, W. Khoury-Hanold, M. Staron, et al., “Mitochondrial DNA Stress Primes the Antiviral Innate Immune Response,” Nature 520, no. 7548 (2015): 553-557.

[394]

E. E. Kesner, A. Saada-Reich, and H. Lorberboum-Galski, “Characteristics of Mitochondrial Transformation Into Human Cells,” Scientific Reports 6 (2016): 26057.

[395]

E. Fernández-Vizarra, G. Ferrín, A. Pérez-Martos, et al., “Isolation of Mitochondria for Biogenetical Studies: An Update,” Mitochondrion 10, no. 3 (2010): 253-262.

[396]

P. C. Liao, C. Bergamini, R. Fato, et al., “Isolation of Mitochondria From Cells and Tissues,” Methods in Cell Biology 155 (2020): 3-31.

[397]

J. A. MacDonald, A. M. Bothun, S. N. Annis, et al., “A Nanoscale, Multi-parametric Flow Cytometry-based Platform to Study Mitochondrial Heterogeneity and Mitochondrial DNA Dynamics,” Communications Biology 2 (2019): 258.

[398]

D. Greiff and M. Myers, “Effect of Dimethyl Sulphoxide on the Cryo-tolerance of Mitochondria,” Nature 190 (1961): 1202-1204.

[399]

V. N. Nukala, I. N. Singh, L. M. Davis, and P. G. Sullivan, “Cryopreservation of Brain Mitochondria: A Novel Methodology for Functional Studies,” Journal of Neuroscience Methods 152, no. 1-2 (2006): 48-54.

[400]

Y. Yamada, M. Ito, M. Arai, et al., “Challenges in Promoting Mitochondrial Transplantation Therapy,” International Journal of Molecular Sciences 21, no. 17 (2020): 6365.

[401]

R. Yamaguchi, A. Andreyev, A. N. Murphy, et al., “Mitochondria Frozen With Trehalose Retain a Number of Biological Functions and Preserve Outer Membrane Integrity,” Cell Death and Differentiation 14, no. 3 (2007): 616-624.

[402]

M. D'Amato, F. Morra, I. Di Meo, and V. Tiranti, “Mitochondrial Transplantation in Mitochondrial Medicine: Current Challenges and Future Perspectives,” International Journal of Molecular Sciences 24, no. 3 (2023): 1969.

[403]

T. G. Zhang and C. Y. Miao, “Mitochondrial Transplantation as a Promising Therapy for Mitochondrial Diseases,” Acta Pharmaceutica Sinica B 13, no. 3 (2023): 1028-1035.

[404]

N. Borcherding, W. Jia, R. Giwa, et al., “Dietary Lipids Inhibit Mitochondria Transfer to Macrophages to Divert Adipocyte-derived Mitochondria Into the Blood,” Cell metabolism 34, no. 10 (2022): 1499-1513. e8.

[405]

J. R. Brestoff, C. B. Wilen, J. R. Moley, et al., “Intercellular Mitochondria Transfer to Macrophages Regulates White Adipose Tissue Homeostasis and Is Impaired in Obesity,” Cell metabolism 33, no. 2 (2021): 270-282. e8.

[406]

J. Xie, Z. Shen, Y. Anraku, et al., “Nanomaterial-based Blood-brain-barrier (BBB) Crossing Strategies,” Biomaterials 224 (2019): 119491.

[407]

A. Aleynik, K. M. Gernavage, Y. S. Mourad, et al., “Stem Cell Delivery of Therapies for Brain Disorders,” Clinical and translational medicine 3 (2014): 24.

[408]

G. Ramirez-Barbieri, K. Moskowitzova, B. Shin, et al., “Alloreactivity and Allorecognition of Syngeneic and Allogeneic Mitochondria,” Mitochondrion 46 (2019): 103-115.

[409]

J. Pollara, R. W. Edwards, L. Lin, et al., “Circulating Mitochondria in Deceased Organ Donors Are Associated With Immune Activation and Early Allograft Dysfunction,” JCI Insight 3, no. 15 (2018): e121622.

[410]

Q. Zhang, M. Raoof, Y. Chen, et al., “Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury,” Nature 464, no. 7285 (2010): 104-107.

[411]

L. Lin, H. Xu, M. Bishawi, et al., “Circulating Mitochondria in Organ Donors Promote Allograft Rejection,” Am J Transplant Off J Am Soc Transplant Am Soc Transpl Surg 19, no. 7 (2019): 1917-1929.

[412]

J. Burrello, S. Monticone, C. Gai, et al., “Stem Cell-Derived Extracellular Vesicles and Immune-Modulation,” Frontiers in Cell and Developmental Biology 4 (2016): 83.

[413]

K. Reinhardt, D. K. Dowling, and E. H. Morrow, “Medicine. Mitochondrial Replacement, Evolution, and the Clinic,” Science 341, no. 6152 (2013): 1345-1346.

[414]

R. Dobler, D. K. Dowling, E. H. Morrow, and K. Reinhardt, “A Systematic Review and Meta-analysis Reveals Pervasive Effects of Germline Mitochondrial Replacement on Components of Health,” Human Reproduction Update 24, no. 5 (2018): 519-534.

[415]

A. Eyre-Walker, “Mitochondrial Replacement Therapy: Are Mito-nuclear Interactions Likely To Be a Problem?,” Genetics 205, no. 4 (2017): 1365-1372.

[416]

R. Gupta, M. Kanai, T. J. Durham, et al., “Nuclear Genetic Control of mtDNA Copy Number and Heteroplasmy in Humans,” Nature 620, no. 7975 (2023): 839-848.

[417]

M. S. Sharpley, C. Marciniak, K. Eckel-Mahan, et al., “Heteroplasmy of Mouse mtDNA Is Genetically Unstable and Results in Altered Behavior and Cognition,” Cell 151, no. 2 (2012): 333-343.

[418]

D. B. Cowan, R. Yao, J. K. Thedsanamoorthy, et al., “Transit and Integration of Extracellular Mitochondria in human Heart Cells,” Scientific Reports 7, no. 1 (2017): 17450.

[419]

A. G. Cox, C. C. Winterbourn, and M. B. Hampton, “Mitochondrial Peroxiredoxin Involvement in Antioxidant Defence and Redox Signalling,” Biochemical Journal 425, no. 2 (2010): 313-325.

RIGHTS & PERMISSIONS

2025 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.

AI Summary AI Mindmap
PDF

121

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/