Sarcopenic obesity: prospects of mitochondrial transplantation to combat metabolic deterioration in aging

Md Ariful Islam , Wenyi Gu , Yijie Song , Yu Xu , Hongxi Xu

Acta Materia Medica ›› 2025, Vol. 4 ›› Issue (3) : 321 -339.

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Acta Materia Medica ›› 2025, Vol. 4 ›› Issue (3) :321 -339. DOI: 10.15212/AMM-2024-0091
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Sarcopenic obesity: prospects of mitochondrial transplantation to combat metabolic deterioration in aging
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Abstract

Aging impairs adipose tissue function and contributes to metabolic disorders, such as obesity and insulin resistance. Chronic inflammation is mediated by cytokines, including IL-6, IL-1β, and TNF-α, is a pivotal factor in aging that links mitochondrial dysfunction to activation of the NLRP3 inflammasome in aged adipose tissue. Moreover, distinct adipose tissue and adipose tissue depots exhibit complex molecular and cellular functions related to the deterioration of conventional metabolic regulation pathways. Unraveling these mechanisms is crucial for developing therapeutic strategies to enhance metabolic health and promote longevity. This review elucidates the current understanding of lipid metabolism, insulin resistance, cellular senescence, and mitochondrial dysfunction. Moreover, strategies to improve mitochondrial quality control in aging adipose tissue, such as mitochondrial transplantation, hold promise for addressing mitochondrial dysfunction. Finally, a novel therapeutic approach for mitochondrial transplantation is proposed using exosome cargo to sustain healthy metabolism and thermogenesis in aging populations. These findings lay the groundwork for innovative therapies and preventive strategies to mitigate the impact of obesity and aging.

Keywords

Adipose tissue / Aging / Inflammation / Insulin Resistance / Cellular Senescence / Mitochondrial transplantation

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Md Ariful Islam, Wenyi Gu, Yijie Song, Yu Xu, Hongxi Xu. Sarcopenic obesity: prospects of mitochondrial transplantation to combat metabolic deterioration in aging. Acta Materia Medica, 2025, 4 (3) : 321-339 DOI:10.15212/AMM-2024-0091

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