Host-microbe co-metabolism system as potential targets: the promising way for natural medicine to treat atherosclerosis

Yun Wang , Ziwei Zhou , Haiping Hao , Lijuan Cao

Chinese Journal of Natural Medicines ›› 2025, Vol. 23 ›› Issue (7) : 790 -800.

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Chinese Journal of Natural Medicines ›› 2025, Vol. 23 ›› Issue (7) :790 -800. DOI: 10.1016/S1875-5364(25)60909-5
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Host-microbe co-metabolism system as potential targets: the promising way for natural medicine to treat atherosclerosis

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Abstract

The host-microbe co-metabolism system, generating diverse exogenous and endogenous bioactive molecules that influence the host’s immune and metabolic functions, plays a crucial role in the pathogenesis of atherosclerosis. Recent studies have elucidated the interaction between natural medicines and this co-metabolism system. Upon oral administration, natural medicine ingredients can undergo transformation by gut microbiota, potentially enhancing their bioavailability or anti-atherogenic efficacy. Furthermore, natural medicines can exert anti-atherogenic effects via modulation of endogenous host-microbe co-metabolism. This review presents an updated understanding of the dual association between natural medicines and host-microbe co-metabolites. It explores the critical function of microbial exogenous metabolites derived from natural medicines and uncovers the mechanisms underlying natural medicines’ intervention on key nodes of endogenous host-microbe co-metabolism. These insights may offer new perspectives for cardiovascular disease (CVD) treatment and guide future drug discovery efforts.

Keywords

Atherosclerosis / Host-microbe co-metabolism system / Natural medicine / Pharmacological mechanisms / Gut microbiota

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Yun Wang, Ziwei Zhou, Haiping Hao, Lijuan Cao. Host-microbe co-metabolism system as potential targets: the promising way for natural medicine to treat atherosclerosis. Chinese Journal of Natural Medicines, 2025, 23(7): 790-800 DOI:10.1016/S1875-5364(25)60909-5

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References

[1]

Herrington W, Lacey B, Sherliker P, et al. Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease. Circ Res. 2016; 118(4):535-546. https://doi.org/10.1161/CIRCRESAHA.115.307611.

[2]

Ralapanawa U, Sivakanesan R. Epidemiology and the magnitude of coronary artery disease and acute coronary syndrome: a narrative review. J Epidemiol Glob Health. 2021; 11(2):169-177. https://doi.org/10.2991/jegh.k.201217.001.

[3]

Mensah GA, Fuster V, Murray CJL, et al.Global burden of cardiovascular diseases and risks, 1990-2022. J Am Coll Cardiol. 2023; 82(25):2350-2473. https://doi.org/10.1016/j.jacc.2023.11.007.

[4]

Jie Z, Xia H, Zhong SL, et al. The gut microbiome in atherosclerotic cardiovascular disease. Nat Commun. 2017; 8(1):845. https://doi.org/10.1038/s41467-017-00900-1.

[5]

Yin J, Liao SX, He Y, et al. Dysbiosis of gut microbiota with reduced trimethylamine-N-oxide level in patients with large-artery atherosclerotic stroke or transient ischemic attack. J Am Heart Assoc. 2015; 4(11):e002699. https://doi.org/10.1161/JAHA.115.002699.

[6]

Dai H, Han J, Wang T, et al. Recent advances in gut microbiota-associated natural products: structures, bioactivities, and mechanisms. Nat Prod Rep. 2023; 40(6):1078-1093. https://doi.org/10.1039/D2NP00075J.

[7]

Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011; 472(7341):57-63. https://doi.org/10.1038/nature09922.

[8]

Nemet I, Saha PP, Gupta N, et al. A cardiovascular disease-linked gut microbial metabolite acts via adrenergic receptors. Cell. 2020; 180(5):862-877. https://doi.org/10.1016/j.cell.2020.02.016.

[9]

Li C, Stražar M, Mohamed AMT, et al. Gut microbiome and metabolome profiling in Framingham heart study reveals cholesterol-metabolizing bacteria. Cell. 2024; 187(8):1834-1852. https://doi.org/10.1016/j.cell.2024.03.014.

[10]

Li TT, Wang ZB, Li Y, et al. The mechanisms of traditional Chinese medicine underlying the prevention and treatment of atherosclerosis. Chin J Nat Med. 2019; 17(6):401-412. https://doi.org/10.1016/S1875-5364(19)30048-2.

[11]

Meng T, Li X, Li C, et al. Natural products of traditional Chinese medicine treat atherosclerosis by regulating inflammatory and oxidative stress pathways. Front Pharmacol. 2022;13:997598. https://doi.org/10.3389/fphar.2022.997598.

[12]

Lin TL, Lu CC, Lai WF, et al. Role of gut microbiota in identification of novel TCM-derived active metabolites. Protein Cell. 2021; 12(5):394-410. https://doi.org/10.1007/s13238-020-00784-w.

[13]

Zhao X, Oduro PK, Tong W, et al. Therapeutic potential of natural products against atherosclerosis: targeting on gut microbiota. Pharmacol Res. 2021;163:105362. https://doi.org/10.1016/j.phrs.2020.105362.

[14]

Yin DF, Zhong YD, Liu H, et al. Lipid metabolism regulation by dietary polysaccharides with different structural properties. Int J Biol Macromol. 2024; 270(Pt 2):132253. https://doi.org/10.1016/j.ijbiomac.2024.132253.

[15]

Chen L, Ge MD, Zhu YJ, et al. Structure, bioactivity and applications of natural hyperbranched polysaccharides. Carbohydr Polym. 2019;223:115076. https://doi.org/10.1016/j.carbpol.2019.115076.

[16]

Yue BJ, Zong GF, Tao RZ, et al. Crosstalk between traditional Chinese medicine-derived polysaccharides and the gut microbiota: a new perspective to understand traditional Chinese medicine. Phytother Res. 2022; 36(11):4125-4138. https://doi.org/10.1002/ptr.7607.

[17]

Wu DT, Fu Y, Guo H, et al. Simulated digestion and fecal fermentation of polysaccharides from loquat leaves: dynamic changes in physicochemical properties and impacts on human gut microbiota. Int J Biol Macromol. 2021; 168:733-742. https://doi.org/10.1016/j.ijbiomac.2020.11.130.

[18]

Wardman JF, Bains RK, Rahfeld P, et al. Carbohydrate-active enzymes (CAZymes) in the gut microbiome. Nat Rev Microbiol. 2022; 20(9):542-556. https://doi.org/10.1038/s41579-022-00712-1.

[19]

Singh RP. Glycan utilisation system in Bacteroides and Bifidobacteria and their roles in gut stability and health. Appl Microbiol Biotechnol. 2019; 103(18):7287-7315. https://doi.org/10.1007/s00253-019-10012-z.

[20]

Fernandez-Julia PJ, Munoz-Munoz J, van Sinderen D. A comprehensive review on the impact of β-glucan metabolism by Bacteroides and Bifidobacterium species as members of the gut microbiota. Int J Biol Macromol. 2021; 181:877-889. https://doi.org/10.1016/j.ijbiomac.2021.04.069.

[21]

Koh A, De Vadder F, Kovatcheva-Datchary P, et al. From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites. Cell. 2016; 165(6):1332-1345. https://doi.org/10.1016/j.cell.2016.05.041.

[22]

Hu TT, Wu QQ, Yao Q, et al. Short-chain fatty acid metabolism and multiple effects on cardiovascular diseases. Ageing Res Rev. 2022;81:101706. https://doi.org/10.1016/j.arr.2022.101706.

[23]

Haghikia A, Zimmermann F, Schumann P, et al. Propionate attenuates atherosclerosis by immune-dependent regulation of intestinal cholesterol metabolism. Eur Heart J. 2022; 43(6):518-533. https://doi.org/10.1093/eurheartj/ehab644.

[24]

Aguilar EC, Leonel AJ, Teixeira LG, et al. Butyrate impairs atherogenesis by reducing plaque inflammation and vulnerability and decreasing NFkappaB activation. Nutr Metab Cardiovasc Dis. 2014; 24(6):606-613. https://doi.org/10.1016/j.numecd.2014.01.002.

[25]

Aguilar EC, dos Santos LC, Leonel AJ, et al. Oral butyrate reduces oxidative stress in atherosclerotic lesion sites by a mechanism involving NADPH oxidase down-regulation in endothelial cells. J Nutr Biochem. 2016; 34:99-105. https://doi.org/10.1016/j.jnutbio.2016.05.002.

[26]

Chen XF, Chen XQ, Tang XQ. Short-chain fatty acid, acylation and cardiovascular diseases. Clin Sci (Lond). 2020; 134(6):657-676. https://doi.org/10.1042/CS20200128.

[27]

Singh N, Gurav A, Sivaprakasam S, et al. Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity. 2014; 40(1):128-139. https://doi.org/10.1016/j.immuni.2013.12.007.

[28]

Liu Z, Xia J, Wang CZ, et al. Remarkable impact of acidic ginsenosides and organic acids on ginsenoside transformation from fresh ginseng to red ginseng. J Agric Food Chem. 2016; 64(26):5389-5399. https://doi.org/10.1021/acs.jafc.6b00963.

[29]

Fan WX, Fan LH, Wang ZY, et al. Rare ginsenosides: a unique perspective of ginseng research. J Adv Res. 2024; 66:303-328. https://doi.org/10.1016/j.jare.2024.01.003.

[30]

Guo YP, Chen MY, Shao L, et al. Quantification of saponins metabolites in rat plasma with gut microbiota-mediated biotransformation by HPLC-MS/MS. Chin J Nat Med. 2019; 17(3):231-240. https://doi.org/10.1016/S1875-5364(19)30026-3.

[31]

Xu QF, Fang XL, Chen DF. Pharmacokinetics and bioavailability of ginsenoside Rb1 and Rg1 from Panax notoginseng in rats. J Ethnopharmacol. 2003; 84(2-3):187-192. https://doi.org/10.1016/S0378-8741(02)00317-3.

[32]

Chu Y, Zhang HC, Li SM, et al. Determination of ginsenoside Rc in rat plasma by LC-MS/MS and its application to a pharmacokinetic study. J Chromatogr B Analyt Technol Biomed Life Sci. 2013; 919:75-78. https://doi.org/10.1016/j.jchromb.2012.12.022.

[33]

Kim DH. Gut microbiota-mediated pharmacokinetics of ginseng saponins. J Ginseng Res. 2018; 42(3):255-263. https://doi.org/10.1016/j.jgr.2017.04.011.

[34]

Yang L, Zou HC, Gao YC, et al. Insights into gastrointestinal microbiota-generated ginsenoside metabolites and their bioactivities. Drug Metab Rev. 2020; 52(1):125-138. https://doi.org/10.1080/03602532.2020.1714645.

[35]

Huang S, Shao L, Chen MY, et al. Biotransformation differences of ginsenoside compound K mediated by the gut microbiota from diabetic patients and healthy subjects. Chin J Nat Med. 2023; 21(10):723-729. https://doi.org/10.1016/S1875-5364(23)60402-9.

[36]

Zhou L, Zheng Y, Li ZY, et al. Compound K attenuates the development of atherosclerosis in ApoE(-/-) mice via LXRα activation. Int J Mol Sci. 2016; 17(7):1054. https://doi.org/10.3390/ijms17071054.

[37]

Huang YW, Zhang M, Wang LT, et al.20(S)-Protopanaxadiol decreases atherosclerosis in ApoE KO mice by increasing the levels of LDLR and inhibiting its binding with PCSK9. Food Funct. 2022; 13(13):7020-7028. https://doi.org/10.1039/D2FO00392A.

[38]

Geng JA, Fu WW, Yu XF, et al. Ginsenoside Rg 3 alleviates ox-LDL induced endothelial dysfunction and prevents atherosclerosis in ApoE-/- mice by regulating PPARγ/FAK signaling pathway. Front Pharmacol. 2020;11:500. https://doi.org/10.3389/fphar.2020.00500.

[39]

Qin M, Luo Y, Lu S, et al. Ginsenoside F 1 ameliorates endothelial cell inflammatory injury and prevents atherosclerosis in mice through A20-mediated suppression of NF-κB signaling. Front Pharmacol. 2017;8:953. https://doi.org/10.3389/fphar.2017.00953.

[40]

Lee SY, Jeong JJ, Eun SH, et al. Anti-inflammatory effects of ginsenoside Rg1 and its metabolites ginsenoside Rh1 and 20(S)-protopanaxatriol in mice with TNBS-induced colitis. Eur J Pharmacol. 2015; 762:333-343. https://doi.org/10.1016/j.ejphar.2015.06.011.

[41]

Lee ES, Choi JS, Kim MS, et al. Ginsenoside metabolite compound K differentially antagonizing tumor necrosis factor-α-induced monocyte-endothelial trafficking. Chem Biol Interact. 2011; 194(1):13-22. https://doi.org/10.1016/j.cbi.2011.08.008.

[42]

Ku YS, Ng MS, Cheng SS, et al. Understanding the composition, biosynthesis, accumulation and transport of flavonoids in crops for the promotion of crops as healthy sources of flavonoids for human consumption. Nutrients. 2020; 12(6):1717. https://doi.org/10.3390/nu12061717.

[43]

Goris T, Cuadrat RRC, Braune A. Flavonoid-modifying capabilities of the human gut microbiome-an in silico study. Nutrients. 2021; 13(8):2688. https://doi.org/10.3390/nu13082688.

[44]

Braune A, Blaut M. Bacterial species involved in the conversion of dietary flavonoids in the human gut. Gut Microbes. 2016; 7(3):216-234. https://doi.org/10.1080/19490976.2016.1158395.

[45]

Yang GH, Hong S, Yang PJ, et al. Discovery of an ene-reductase for initiating flavone and flavonol catabolism in gut bacteria. Nat Commun. 2021; 12(1):790. https://doi.org/10.1038/s41467-021-20974-2.

[46]

Chalet C, Hollebrands B, Janssen HG, et al. Identification of phase-II metabolites of flavonoids by liquid chromatography-ion-mobility spectrometry-mass spectrometry. Anal Bioanal Chem. 2018; 410(2):471-482. https://doi.org/10.1007/s00216-017-0737-4.

[47]

Li HX, Cao ZQ, Liu C, et al. Quercetin inhibits neuronal pyroptosis and ferroptosis by modulating microglial M1/M2 polarization in atherosclerosis. J Agric Food Chem. 2024; 72(21):12156-12170. https://doi.org/10.1021/acs.jafc.4c01134.

[48]

Feng Z, Wang CY, Yue J, et al. Kaempferol-induced GPER upregulation attenuates atherosclerosis via the PI3K/AKT/Nrf2 pathway. Pharm Biol. 2021; 59(1):1106-1116. https://doi.org/10.1080/13880209.2021.1961823.

[49]

Weng XZ, Luo X, Dai XY, et al. Apigenin inhibits macrophage pyroptosis through regulation of oxidative stress and the NF-κB pathway and ameliorates atherosclerosis. Phytother Res. 2023; 37(11):5300-5314. https://doi.org/10.1002/ptr.7962.

[50]

Assini JM, Mulvihill EE, Sutherland BG, et al. Naringenin prevents cholesterol-induced systemic inflammation, metabolic dysregulation, and atherosclerosis in Ldlr-/- mice. J Lipid Res. 2013; 54(3):711-724. https://doi.org/10.1194/jlr.M032631.

[51]

Xu XT, Lei TW, Li WC, et al. Enhanced cellular cholesterol efflux by naringenin is mediated through inhibiting endoplasmic reticulum stress-ATF6 activity in macrophages. Biochim Biophys Acta Mol Cell Biol Lipids. 2019; 1864(10):1472-1482. https://doi.org/10.1016/j.bbalip.2019.06.005.

[52]

Ding M, Zhu Y, Xu XT, et al. Naringenin inhibits acid sphingomyelinase-mediated membrane raft clustering to reduce NADPH oxidase activation and vascular inflammation. J Agric Food Chem. 2024; 72(13):7130-7139. https://doi.org/10.1021/acs.jafc.3c07874.

[53]

Qin WW, Ren B, Wang SS, et al. Apigenin and naringenin ameliorate PKCβII-associated endothelial dysfunction regulating ROS/caspase-3 and NO pathway in endothelial cells exposed to high glucose. Vascul Pharmacol. 2016; 85:39-49. https://doi.org/10.1016/j.vph.2016.07.006.

[54]

Kim MS, Park SH, Han SY, et al.Phloretin suppresses thrombin-mediated leukocyte-platelet-endothelial interactions. Mol Nutr Food Res. 2014; 58(4):698-708. https://doi.org/10.1002/mnfr.201300267.

[55]

Stangl V, Lorenz M, Ludwig A, et al. The flavonoid phloretin suppresses stimulated expression of endothelial adhesion molecules and reduces activation of human platelets. J Nutr. 2005; 135(2):172-178. https://doi.org/10.1093/jn/135.2.172.

[56]

Lee CC, Kim JH, Kim JS, et al. 5-(3′4′-Dihydroxyphenyl-γ-valerolactone), a major microbial metabolite of proanthocyanidin, attenuates THP-1 monocyte-endothelial adhesion. Int J Mol Sci. 2017; 18(7):1363. https://doi.org/10.3390/ijms18071363.

[57]

Mena P, Bresciani L, Brindani N, et al. Phenyl-γ-valerolactones and phenylvaleric acids, the main colonic metabolites of flavan-3-ols: synthesis, analysis, bioavailability, and bioactivity. Nat Prod Rep. 2019; 36(5):714-752. https://doi.org/10.1039/C8NP00062J.

[58]

Kutschera M, Engst W, Blaut M, et al. Isolation of catechin-converting human intestinal bacteria. J Appl Microbiol. 2011; 111(1):165-175. https://doi.org/10.1111/j.1365-2672.2011.05025.x.

[59]

Sánchez-Patán F, Tabasco R, Monagas M, et al. Capability of Lactobacillus plantarum IFPL935 to catabolize flavan-3-ol compounds and complex phenolic extracts. J Agric Food Chem. 2012; 60(29):7142-7151. https://doi.org/10.1021/jf3006867.

[60]

Lotito SB, Zhang WJ, Yang CS, et al. Metabolic conversion of dietary flavonoids alters their anti-inflammatory and antioxidant properties. Free Radic Biol Med. 2011; 51(2):454-463. https://doi.org/10.1016/j.freeradbiomed.2011.04.032.

[61]

Lee CC, Dudonné S, Kim JH, et al. A major daidzin metabolite 7,8,4′-trihydroxyisoflavone found in the plasma of soybean extract-fed rats attenuates monocyte-endothelial cell adhesion. Food Chem. 2018; 240:607-614. https://doi.org/10.1016/j.foodchem.2017.08.002.

[62]

Zeisel SH, Warrier M. Trimethylamine N-oxide, the microbiome, and heart and kidney disease. Annu Rev Nutr. 2017; 37:157-181. https://doi.org/10.1146/annurev-nutr-071816-064732.

[63]

Ma SR, Tong Q, Lin Y, et al. Berberine treats atherosclerosis via a vitamine-like effect down-regulating choline-TMA-TMAO production pathway in gut microbiota. Signal Transduct Target Ther. 2022; 7(1):207. https://doi.org/10.1038/s41392-022-01027-6.

[64]

Li SXM, Obeid S, Klingenberg R, et al. Gut microbiota-dependent trimethylamine N-oxide in acute coronary syndromes: a prognostic marker for incident cardiovascular events beyond traditional risk factors. Eur Heart J. 2017; 38(11):814-824. https://doi.org/10.1093/eurheartj/ehw582.

[65]

Koeth RA, Wang Z, Levison BS, et al. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med. 2013; 19(5):576-585. https://doi.org/10.1038/nm.3145.

[66]

Romano KA, Vivas EI, Amador-Noguez D, et al. Intestinal microbiota composition modulates choline bioavailability from diet and accumulation of the proatherogenic metabolite trimethylamine-N-oxide. mBio. 2015; 6(2):e02481. https://doi.org/10.1128/mBio.02481-14.

[67]

Yoo W, Zieba JK, Foegeding NJ, et al. High-fat diet-induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide. Science. 2021; 373(6556):813-818. https://doi.org/10.1126/science.aba3683.

[68]

Cai YY, Huang FQ, Lao X, et al. Integrated metagenomics identifies a crucial role for trimethylamine-producing Lachnoclostridium in promoting atherosclerosis. NPJ Biofilms Microbiomes. 2022; 8(1):11. https://doi.org/10.1038/s41522-022-00273-4.

[69]

Craciun S, Balskus EP. Microbial conversion of choline to trimethylamine requires a glycyl radical enzyme. Proc Natl Acad Sci U S A. 2012; 109(52):21307-21312. https://doi.org/10.1073/pnas.1215689109.

[70]

Zhu Y, Jameson E, Crosatti M, et al. Carnitine metabolism to trimethylamine by an unusual Rieske-type oxygenase from human microbiota. Proc Natl Acad Sci U S A. 2014; 111(11):4268-4273. https://doi.org/10.1073/pnas.1316569111.

[71]

Koeth RA, Levison BS, Culley MK, et al. γ-Butyrobetaine is a proatherogenic intermediate in gut microbial metabolism of L-carnitine to TMAO. Cell Metab. 2014; 20(5):799-812. https://doi.org/10.1016/j.cmet.2014.10.006.

[72]

Wu K, Yuan Y, Yu H, et al. The gut microbial metabolite trimethylamine N-oxide aggravates GVHD by inducing M1 macrophage polarization in mice. Blood. 2020; 136(4):501-515. https://doi.org/10.1182/blood.2019003990.

[73]

Zhang X, Li Y, Yang P, et al. Trimethylamine-N-oxide promotes vascular calcification through activation of NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome and NF-κB (nuclear factor κB) signals. Arterioscler Thromb Vasc Biol. 2020; 40(3):751-765. https://doi.org/10.1161/ATVBAHA.119.313414.

[74]

Sun X, Jiao X, Ma Y, et al. Trimethylamine N-oxide induces inflammation and endothelial dysfunction in human umbilical vein endothelial cells via activating ROS-TXNIP-NLRP3 inflammasome. Biochem Biophys Res Commun. 2016; 481(1-2):63-70. https://doi.org/10.1016/j.bbrc.2016.11.017.

[75]

Zhu W, Gregory JC, Org E, et al. Gut microbial metabolite TMAO enhances platelet hyperreactivity and thrombosis risk. Cell. 2016; 165(1):111-124. https://doi.org/10.1016/j.cell.2016.02.011.

[76]

Cheng CK, Luo JY, Lau CW, et al. Pharmacological basis and new insights of resveratrol action in the cardiovascular system. Br J Pharmacol. 2020; 177(6):1258-1277. https://doi.org/10.1111/bph.14801.

[77]

Hao H, Zheng X, Wang G. Insights into drug discovery from natural medicines using reverse pharmacokinetics. Trends Pharmacol Sci. 2014; 35(4):168-177. https://doi.org/10.1016/j.tips.2014.02.001.

[78]

Chen ML, Yi L, Zhang Y, et al. Resveratrol attenuates trimethylamine-N-oxide (TMAO)-induced atherosclerosis by regulating TMAO synthesis and bile acid metabolism via remodeling of the gut microbiota. mBio. 2016; 7(2):e02210-02215. https://doi.org/10.1128/mBio.02210-15.

[79]

Ju J, Li J, Lin Q, et al. Efficacy and safety of berberine for dyslipidaemias: a systematic review and meta-analysis of randomized clinical trials. Phytomedicine. 2018; 50:25-34. https://doi.org/10.1016/j.phymed.2018.09.212.

[80]

Wang K, Feng X, Chai L, et al. The metabolism of berberine and its contribution to the pharmacological effects. Drug Metab Rev. 2017; 49(2):139-157. https://doi.org/10.1080/03602532.2017.1306544.

[81]

Shi Y, Hu J, Geng J, et al. Berberine treatment reduces atherosclerosis by mediating gut microbiota in apoE-/- mice. Biomed Pharmacother. 2018; 107:1556-1563. https://doi.org/10.1016/j.biopha.2018.08.148.

[82]

Li X, Su C, Jiang Z, et al. Berberine attenuates choline-induced atherosclerosis by inhibiting trimethylamine and trimethylamine-N-oxide production via manipulating the gut microbiome. NPJ Biofilms Microbiomes. 2021; 7(1):36. https://doi.org/10.1038/s41522-021-00205-8.

[83]

Zhu L, Zhang D, Zhu H, et al. Berberine treatment increases Akkermansia in the gut and improves high-fat diet-induced atherosclerosis in Apoe(-/-) mice. Atherosclerosis. 2018; 268:117-126. https://doi.org/10.1016/j.atherosclerosis.2017.11.023.

[84]

Chen Y, Hao Z, Zhao H, et al. Berberine alleviates intestinal barrier dysfunction in glucolipid metabolism disorder hamsters by modulating gut microbiota and gut-microbiota-related tryptophan metabolites. J Sci Food Agric. 2023; 103(3):1464-1473. https://doi.org/10.1002/jsfa.12242.

[85]

Panyod S, Wu WK, Chen PC, et al. Atherosclerosis amelioration by allicin in raw garlic through gut microbiota and trimethylamine-N-oxide modulation. NPJ Biofilms Microbiomes. 2022; 8(1):4. https://doi.org/10.1038/s41522-022-00266-3.

[86]

Zhang J, Ou C, Chen M. Curcumin attenuates cadmium-induced atherosclerosis by regulating trimethylamine-N-oxide synthesis and macrophage polarization through remodeling the gut microbiota. Ecotoxicol Environ Saf. 2022;244:114057. https://doi.org/10.1016/j.ecoenv.2022.114057.

[87]

Lin K, Wang X, Li J, et al. Anti-atherosclerotic effects of geraniin through the gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway in mice. Phytomedicine. 2022;101:154104. https://doi.org/10.1016/j.phymed.2022.154104.

[88]

Li ZH, Weng J, Yan J, et al. Puerarin alleviates atherosclerosis via the inhibition of Prevotella copri and its trimethylamine production. Gut. 2024; 73(12):1934-1943. https://doi.org/10.1136/gutjnl-2024-331880.

[89]

Liu S, He F, Zheng T, et al. Ligustrum robustum alleviates atherosclerosis by decreasing serum TMAO, modulating gut microbiota, and decreasing bile acid and cholesterol absorption in mice. Mol Nutr Food Res. 2021; 65(14):e2100014. https://doi.org/10.1002/mnfr.202100014.

[90]

Panyod S, Wu WK, Peng SY, et al. Ginger essential oil and citral ameliorates atherosclerosis in ApoE(-/-) mice by modulating trimethylamine-N-oxide and gut microbiota. NPJ Sci Food. 2023; 7(1):19. https://doi.org/10.1038/s41538-023-00196-0.

[91]

Wang Z, Roberts AB, Buffa JA, et al. Non-lethal inhibition of gut microbial trimethylamine production for the treatment of atherosclerosis. Cell. 2015; 163(7):1585-1595. https://doi.org/10.1016/j.cell.2015.11.055.

[92]

Lee H, Liu X, An JP, et al. Identification of polymethoxyflavones (PMFs) from orange peel and their inhibitory effects on the formation of trimethylamine (TMA) and trimethylamine-N-oxide (TMAO) using cntA/B and cutC/D enzymes and molecular docking. J Agric Food Chem. 2023; 71(43):16114-16124. https://doi.org/10.1021/acs.jafc.3c04462.

[93]

Zhou P, Zhao XN, Ma YY, et al. Virtual screening analysis of natural flavonoids as trimethylamine (TMA)-lyase inhibitors for coronary heart disease. J Food Biochem. 2022; 46(12):e14376. https://doi.org/10.1111/jfbc.14376.

[94]

Jiang C, Wang S, Wang Y, et al. Polyphenols from hickory nut reduce the occurrence of atherosclerosis in mice by improving intestinal microbiota and inhibiting trimethylamine N-oxide production. Phytomedicine. 2024;128:155349. https://doi.org/10.1016/j.phymed.2024.155349.

[95]

Lv Z, Shan X, Tu Q, et al. Ginkgolide B treatment regulated intestinal flora to improve high-fat diet induced atherosclerosis in ApoE(-/-) mice. Biomed Pharmacother. 2021;134:111100. https://doi.org/10.1016/j.biopha.2020.111100.

[96]

Yang Q, Xu Y, Shen L, et al. Guanxinning Tablet attenuates coronary atherosclerosis via regulating the gut microbiota and their metabolites in tibetan minipigs induced by a high-fat diet. J Immunol Res. 2022;2022:7128230. https://doi.org/10.1155/2022/7128230.

[97]

Zhu B, Zhai Y, Ji M, et al. Alisma orientalis beverage treats atherosclerosis by regulating gut microbiota in ApoE(-/-) mice. Front Pharmacol. 2020;11:570555. https://doi.org/10.3389/fphar.2020.570555.

[98]

Perino A, Schoonjans K.Metabolic messengers: bile acids. Nat Metab. 2022; 4(4):416-423. https://doi.org/10.1038/s42255-022-00559-z.

[99]

Deo AK, Bandiera SM. Identification of human hepatic cytochrome p450 enzymes involved in the biotransformation of cholic and chenodeoxycholic acid. Drug Metab Dispos. 2008; 36(10):1983-1991. https://doi.org/10.1124/dmd.108.022194.

[100]

Takahashi S, Fukami T, Masuo Y, et al. Cyp2c70 is responsible for the species difference in bile acid metabolism between mice and humans. J Lipid Res. 2016; 57(12):2130-2137. https://doi.org/10.1194/jlr.M071183.

[101]

Russell DW. Fifty years of advances in bile acid synthesis and metabolism. J Lipid Res. 2009;50(Suppl):S120-S125. https://doi.org/10.1194/jlr.R800026-JLR200.

[102]

Chiang JY.Bile acid metabolism and signaling. Compr Physiol. 2013; 3(3):1191-1212. https://doi.org/10.1002/cphy.c120023.

[103]

Gonzalez FJ. Nuclear receptor control of enterohepatic circulation. Compr Physiol. 2012; 2(4):2811-2828. https://doi.org/10.1002/cphy.c120007.

[104]

Winston JA, Theriot CM. Diversification of host bile acids by members of the gut microbiota. Gut Microbes. 2020; 11(2):158-171. https://doi.org/10.1080/19490976.2019.1674124.

[105]

Jones BV, Begley M, Hill C, et al. Functional and comparative metagenomic analysis of bile salt hydrolase activity in the human gut microbiome. Proc Natl Acad Sci U S A. 2008; 105(36):13580-13585. https://doi.org/10.1073/pnas.0804437105.

[106]

Song Z, Cai Y, Lao X, et al. Taxonomic profiling and populational patterns of bacterial bile salt hydrolase (BSH) genes based on worldwide human gut microbiome. Microbiome. 2019; 7(1):9. https://doi.org/10.1186/s40168-019-0628-3.

[107]

Su X, Gao Y, Yang R. Gut microbiota derived bile acid metabolites maintain the homeostasis of gut and systemic immunity. Front Immunol. 2023;14:1127743. https://doi.org/10.3389/fimmu.2023.1127743.

[108]

Cai J, Sun L, Gonzalez FJ. Gut microbiota-derived bile acids in intestinal immunity, inflammation, and tumorigenesis. Cell Host Microbe. 2022; 30(3):289-300. https://doi.org/10.1016/j.chom.2022.02.004.

[109]

Wise JL, Cummings BP. The 7-α-dehydroxylation pathway: an integral component of gut bacterial bile acid metabolism and potential therapeutic target. Front Microbiol. 2023;13:1093420. https://doi.org/10.3389/fmicb.2022.1093420.

[110]

Vital M, Rud T, Rath S, et al. Diversity of bacteria exhibiting bile acid-inducible 7α-dehydroxylation genes in the human gut. Comput Struct Biotechnol J. 2019; 17:1016-1019. https://doi.org/10.1016/j.csbj.2019.07.012.

[111]

Streidl T, Karkossa I, Segura Muñoz RR, et al. The gut bacterium Extibacter muris produces secondary bile acids and influences liver physiology in gnotobiotic mice. Gut Microbes. 2021; 13(1):1-21. https://doi.org/10.1080/19490976.2020.1854008.

[112]

White BA, Fricke RJ, Hylemon PB. 7beta-Dehydroxylation of ursodeoxycholic acid by whole cells and cell extracts of the intestinal anaerobic bacterium, Eubacterium species V. P. I. 12708. J Lipid Res. 1982; 23(1):145-153. https://doi.org/10.1016/S0022-2275(20)38183-9.

[113]

Eyssen HJ, De Pauw G, Van Eldere J. Formation of hyodeoxycholic acid from muricholic acid and hyocholic acid by an unidentified gram-positive rod termed HDCA-1 isolated from rat intestinal microflora. Appl Environ Microbiol. 1999; 65(7):3158-3163. https://doi.org/10.1128/AEM.65.7.3158-3163.1999.

[114]

Ridlon JM, Kang DJ, Hylemon PB. Bile salt biotransformations by human intestinal bacteria. J Lipid Res. 2006; 47(2):241-259. https://doi.org/10.1194/jlr.R500013-JLR200.

[115]

Zheng MM, Wang RF, Li CX, et al.Two-step enzymatic synthesis of ursodeoxycholic acid with a new 7β-hydroxysteroid dehydrogenase from Ruminococcus torques. Process Biochem. 2015; 50(4):598-604. https://doi.org/10.1016/j.procbio.2014.12.026.

[116]

Rajani C, Jia W. Bile acids and their effects on diabetes. Front Med. 2018; 12(6):608-623. https://doi.org/10.1007/s11684-018-0644-x.

[117]

Goodwin B, Jones SA, Price RR, et al. A regulatory cascade of the nuclear receptors FXR, SHP-1, and LRH-1 represses bile acid biosynthesis. Mol Cell. 2000; 6(3):517-526. https://doi.org/10.1016/S1097-2765(00)00051-4.

[118]

Collins SL, Stine JG, Bisanz JE, et al. Bile acids and the gut microbiota: metabolic interactions and impacts on disease. Nat Rev Microbiol. 2023; 21(4):236-247. https://doi.org/10.1038/s41579-022-00805-x.

[119]

Xu Y, Li F, Zalzala M, et al. Farnesoid X receptor activation increases reverse cholesterol transport by modulating bile acid composition and cholesterol absorption in mice. Hepatology. 2016; 64(4):1072-1085. https://doi.org/10.1002/hep.28712.

[120]

Wu Q, Sun L, Hu X, et al. Suppressing the intestinal farnesoid X receptor/sphingomyelin phosphodiesterase 3 axis decreases atherosclerosis. J Clin Invest. 2021; 131(9):e142865. https://doi.org/10.1172/JCI142865.

[121]

de Boer JF, Schonewille M, Boesjes M, et al. Intestinal farnesoid X receptor controls transintestinal cholesterol excretion in mice. Gastroenterology. 2017; 152(5):1126-1138. https://doi.org/10.1053/j.gastro.2016.12.037.

[122]

Jiang C, Xie C, Li F, et al. Intestinal farnesoid X receptor signaling promotes nonalcoholic fatty liver disease. J Clin Invest. 2015; 125(1):386-402. https://doi.org/10.1172/JCI76738.

[123]

Pols TW, Nomura M, Harach T, et al. TGR5 activation inhibits atherosclerosis by reducing macrophage inflammation and lipid loading. Cell Metab. 2011; 14(6):747-757. https://doi.org/10.1016/j.cmet.2011.11.006.

[124]

Makishima M, Okamoto AY, Repa JJ, et al. Identification of a nuclear receptor for bile acids. Science. 1999; 284(5418):1362-1365. https://doi.org/10.1126/science.284.5418.1362.

[125]

Li F, Jiang C, Krausz KW, et al. Microbiome remodelling leads to inhibition of intestinal farnesoid X receptor signalling and decreased obesity. Nat Commun. 2013;4:2384. https://doi.org/10.1038/ncomms3384.

[126]

Zheng X, Chen T, Jiang R, et al. Hyocholic acid species improve glucose homeostasis through a distinct TGR5 and FXR signaling mechanism. Cell Metab. 2021; 33(4):791-803. https://doi.org/10.1016/j.cmet.2020.11.017.

[127]

Jin W, Zheng M, Chen Y, et al. Update on the development of TGR5 agonists for human diseases. Eur J Med Chem. 2024;271:116462. https://doi.org/10.1016/j.ejmech.2024.116462.

[128]

Schoeler M, Caesar R. Dietary lipids, gut microbiota and lipid metabolism. Rev Endocr Metab Disord. 2019; 20(4):461-472. https://doi.org/10.1007/s11154-019-09512-0.

[129]

Luna-Marco C, de Marañon AM, Hermo-Argibay A, et al. Effects of GLP-1 receptor agonists on mitochondrial function, inflammatory markers and leukocyte-endothelium interactions in type 2 diabetes. Redox Biol. 2023;66:102849. https://doi.org/10.1016/j.redox.2023.102849.

[130]

Huang K, Liu C, Peng M, et al. Glycoursodeoxycholic acid ameliorates atherosclerosis and alters gut microbiota in apolipoprotein E-deficient mice. J Am Heart Assoc. 2021; 10(7):e019820. https://doi.org/10.1161/JAHA.120.019820.

[131]

Sehayek E, Ono JG, Duncan EM, et al. Hyodeoxycholic acid efficiently suppresses atherosclerosis formation and plasma cholesterol levels in mice. J Lipid Res. 2001; 42(8):1250-1256. https://doi.org/10.1016/S0022-2275(20)31575-3.

[132]

Shih DM, Shaposhnik Z, Meng Y, et al. Hyodeoxycholic acid improves HDL function and inhibits atherosclerotic lesion formation in LDLR-knockout mice. FASEB J. 2013; 27(9):3805-3817. https://doi.org/10.1096/fj.12-223008.

[133]

Hang S, Paik D, Yao L, et al. Bile acid metabolites control T(H)17 and T(reg) cell differentiation. Nature. 2019; 576(7785):143-148. https://doi.org/10.1038/s41586-019-1785-z.

[134]

Paik D, Yao L, Zhang Y, et al. Human gut bacteria produce TH17-modulating bile acid metabolites. Nature. 2022; 603(7903):907-912. https://doi.org/10.1038/s41586-022-04480-z.

[135]

Hao H, Cao L, Jiang C, et al. Farnesoid X receptor regulation of the NLRP3 inflammasome underlies cholestasis-associated sepsis. Cell Metab. 2017; 25(4):856-867. https://doi.org/10.1016/j.cmet.2017.03.007.

[136]

Xu W, Che Y, Zhang Q, et al. Apaf-1 pyroptosome senses mitochondrial permeability transition. Cell Metab. 2021; 33(2):424-436.e10. https://doi.org/10.1016/j.cmet.2020.11.018.

[137]

Che Y, Xu W, Ding C, et al. Bile acids target mitofusin 2 to differentially regulate innate immunity in physiological versus cholestatic conditions. Cell Rep. 2023; 42(1):112011. https://doi.org/10.1016/j.celrep.2023.112011.

[138]

Ding C, Hong Y, Che Y, et al. Bile acid restrained T cell activation explains cholestasis aggravated hepatitis B virus infection. FASEB J. 2022; 36(9):e22468. https://doi.org/10.1096/fj.202200332R.

[139]

Chung J, An SH, Kang SW, et al. Ursodeoxycholic acid (UDCA) exerts anti-atherogenic effects by inhibiting RAGE signaling in diabetic atherosclerosis. PLoS One. 2016; 11(1):e0147839. https://doi.org/10.1371/journal.pone.0147839.

[140]

Chung J, Kim KH, Lee SC, et al. Ursodeoxycholic acid (UDCA) exerts anti-atherogenic effects by inhibiting endoplasmic reticulum (ER) stress induced by disturbed flow. Mol Cells. 2015; 38(10):851-858. https://doi.org/10.14348/molcells.2015.0094.

[141]

Yamamoto M, Uemura T, Nakama S, et al. Serum HDL-cholesterol-increasing and fatty liver-improving actions of Panax ginseng in high cholesterol diet-fed rats with clinical effect on hyperlipidemia in man. Am J Chin Med. 1983; 11(1-4):96-101. https://doi.org/10.1142/S0192415X83000161.

[142]

Wang Y, Wu J, Hong Y, et al. Ginsenosides retard atherogenesis via remodelling host-microbiome metabolic homeostasis. Br J Pharmacol. 2024; 181(12):1768-1792. https://doi.org/10.1111/bph.16320.

[143]

Shen J, Guo H, Liu S, et al. Aberrant branched-chain amino acid accumulation along the microbiota-gut-brain axis: crucial targets affecting the occurrence and treatment of ischaemic stroke. Br J Pharmacol. 2023; 180(3):347-368. https://doi.org/10.1111/bph.15965.

[144]

Watanabe S, Katsube T, Hattori H, et al. Effect of Lactobacillus brevis 119-2 isolated from Tsuda Kabu red turnips on cholesterol levels in cholesterol-administered rats. J Biosci Bioeng. 2013; 116(1):45-51. https://doi.org/10.1016/j.jbiosc.2013.01.009.

[145]

Tian F, Huang S, Xu W, et al. Compound K attenuates hyperglycemia by enhancing glucagon-like peptide-1 secretion through activating TGR5 via the remodeling of gut microbiota and bile acid metabolism. J Ginseng Res. 2022; 46(6):780-789. https://doi.org/10.1016/j.jgr.2022.03.006.

[146]

Quan LH, Zhang C, Dong M, et al. Myristoleic acid produced by enterococci reduces obesity through brown adipose tissue activation. Gut. 2020; 69(7):1239-1247. https://doi.org/10.1136/gutjnl-2019-319114.

[147]

Zhu Y, Li T, Din AU, et al. Beneficial effects of Enterococcus faecalis in hypercholesterolemic mice on cholesterol transportation and gut microbiota. Appl Microbiol Biotechnol. 2019; 103(7):3181-3191. https://doi.org/10.1007/s00253-019-09681-7.

[148]

Bird JK, Raederstorff D, Weber P, et al. Cardiovascular and antiobesity effects of resveratrol mediated through the gut microbiota. Adv Nutr. 2017; 8(6):839-849. https://doi.org/10.3945/an.117.016568.

[149]

Wang F, Zhao C, Tian G, et al. Naringin alleviates atherosclerosis in ApoE(-/-) mice by regulating cholesterol metabolism involved in gut microbiota remodeling. J Agric Food Chem. 2020; 68(45):12651-12660. https://doi.org/10.1021/acs.jafc.0c05800.

[150]

Wang F, Zhao C, Yang M, et al. Four citrus flavanones exert atherosclerosis alleviation effects in ApoE(-/-) mice via different metabolic and signaling pathways. J Agric Food Chem. 2021; 69(17):5226-5237. https://doi.org/10.1021/acs.jafc.1c01463.

[151]

Zhao S, Rong C, Gao Y, et al. Antidepressant-like effect of Ganoderma lucidum spore polysaccharide-peptide mediated by upregulation of prefrontal cortex brain-derived neurotrophic factor. Appl Microbiol Biotechnol. 2021; 105(23):8675-8688. https://doi.org/10.1007/s00253-021-11634-y.

[152]

Xu Y, Zhang X, Yan XH, et al. Characterization, hypolipidemic and antioxidant activities of degraded polysaccharides from Ganoderma lucidum. Int J Biol Macromol. 2019; 135:706-716. https://doi.org/10.1016/j.ijbiomac.2019.05.166.

[153]

Li YH, Tang J, Gao HL, et al. Ganoderma lucidum triterpenoids and polysaccharides attenuate atherosclerotic plaque in high-fat diet rabbits. Nutr Metab Cardiovasc Dis. 2021; 31(6):1929-1938. https://doi.org/10.1016/j.numecd.2021.03.023.

[154]

Romero-Córdoba SL, Salido-Guadarrama I, Meneses ME, et al. Mexican Ganoderma lucidum extracts decrease lipogenesis modulating transcriptional metabolic networks and gut microbiota in C57BL/6 mice fed with a high-cholesterol diet. Nutrients. 2020; 13(1):38. https://doi.org/10.3390/nu13010038.

[155]

Qiao S, Liu C, Sun L, et al. Gut Parabacteroides merdae protects against cardiovascular damage by enhancing branched-chain amino acid catabolism. Nat Metab. 2022; 4(10):1271-1286. https://doi.org/10.1038/s42255-022-00649-y.

[156]

Chang CJ, Lin CS, Lu CC, et al. Ganoderma lucidum reduces obesity in mice by modulating the composition of the gut microbiota. Nat Commun. 2015;6:7489. https://doi.org/10.1038/ncomms8489.

[157]

Kasahara K, Krautkramer KA, Org E, et al. Interactions between Roseburia intestinalis and diet modulate atherogenesis in a murine model. Nat Microbiol. 2018; 3(12):1461-1471. https://doi.org/10.1038/s41564-018-0272-x.

[158]

Wang Y, Xu Y, Xu X, et al. Ginkgo biloba extract ameliorates atherosclerosis via rebalancing gut flora and microbial metabolism. Phytother Res. 2022; 36(6):2463-2480. https://doi.org/10.1002/ptr.7439.

[159]

Wang A, Guan B, Shao C, et al. Qing-Xin-Jie-Yu Granule alleviates atherosclerosis by reshaping gut microbiota and metabolic homeostasis of ApoE-/- mice. Phytomedicine. 2022;103:154220. https://doi.org/10.1016/j.phymed.2022.154220.

[160]

Nemet I, Li XS, Haghikia A, et al. Atlas of gut microbe-derived products from aromatic amino acids and risk of cardiovascular morbidity and mortality. Eur Heart J. 2023; 44(32):3085-3096. https://doi.org/10.1093/eurheartj/ehad333.

[161]

Liu YL, Hou YL, Wang GJ, et al. Gut Microbial Metabolites of Aromatic Amino Acids as Signals in Host-Microbe Interplay. Trends Endocrinol Metab. 2020; 31(11):818-834. https://doi.org/10.1016/j.tem.2020.02.012.

[162]

Nemet I, Funabashi M, Li XS, et al. Microbe-derived uremic solutes enhance thrombosis potential in the host. mBio. 2023; 14(6):e0133123. https://doi.org/10.1128/mbio.01331-23.

[163]

Machado RTR, Brito CB, Byndloss MX. Can our microbiome break our hearts? Collaborative production of p-cresol sulfate and indoxyl sulfate by commensal microbes increases susceptibility to thrombosis. mBio. 2024; 15(2):e0269223. https://doi.org/10.1128/mbio.02692-23.

[164]

Chaves LD, Abyad S, Honan AM, et al. Unconjugated p-cresol activates macrophage macropinocytosis leading to increased LDL uptake. JCI Insight. 2021; 6(11):e144410. https://doi.org/10.1172/jci.insight.144410.

[165]

Jing YJ, Ni JW, Ding FH, et al. p-Cresyl sulfate is associated with carotid arteriosclerosis in hemodialysis patients and promotes atherogenesis in apoE-/- mice. Kidney Int. 2016; 89(2):439-449. https://doi.org/10.1038/ki.2015.287.

[166]

Chang MC, Chang HH, Chan CP, et al. p-Cresol affects reactive oxygen species generation, cell cycle arrest, cytotoxicity and inflammation/atherosclerosis-related modulators production in endothelial cells and mononuclear cells. PLoS One. 2014; 9(12):e114446. https://doi.org/10.1371/journal.pone.0114446.

[167]

Han H, Chen Y, Zhu Z, et al. p-Cresyl sulfate promotes the formation of atherosclerotic lesions and induces plaque instability by targeting vascular smooth muscle cells. Front Med. 2016; 10(3):320-329. https://doi.org/10.1007/s11684-016-0463-x.

[168]

Graboski AL, Kowalewski ME, Simpson JB, et al. Mechanism-based inhibition of gut microbial tryptophanases reduces serum indoxyl sulfate. Cell Chem Biol. 2023; 30(11):1402-1413. https://doi.org/10.1016/j.chembiol.2023.07.015.

[169]

Lu C, Wu L, Tang MY, et al.Indoxyl sulfate in atherosclerosis. Toxicol Lett. 2023; 383:204-212. https://doi.org/10.1016/j.toxlet.2023.07.001.

[170]

Yang K, Du C, Wang X, et al. Indoxyl sulfate induces platelet hyperactivity and contributes to chronic kidney disease-associated thrombosis in mice. Blood. 2017; 129(19):2667-2679. https://doi.org/10.1182/blood-2016-10-744060.

[171]

Nakano T, Katsuki S, Chen M, et al. Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation via the interplay of OATP2B1 and Dll4-Notch signaling. Circulation. 2019; 139(1):78-96. https://doi.org/10.1161/CIRCULATIONAHA.118.034588.

[172]

Zhu Y, Dwidar M, Nemet I, et al. Two distinct gut microbial pathways contribute to meta-organismal production of phenylacetylglutamine with links to cardiovascular disease. Cell Host Microbe. 2023; 31(1):18-32. https://doi.org/10.1016/j.chom.2022.11.015.

[173]

Krishnamoorthy NK, Kalyan M, Hediyal TA, et al. Role of the gut bacteria-derived metabolite phenylacetylglutamine in health and diseases. ACS Omega. 2024; 9(3):3164-3172. https://doi.org/10.1021/acsomega.3c08184.

[174]

Oikawa D, Yamashita S, Takahashi S, et al. (+)-Sesamin, a sesame lignan, is a potent inhibitor of gut bacterial tryptophan indole-lyase that is a key enzyme in chronic kidney disease pathogenesis. Biochem Biophys Res Commun. 2022; 590:158-162. https://doi.org/10.1016/j.bbrc.2021.12.088.

[175]

Sakanaka S, Okada Y. Inhibitory effects of green tea polyphenols on the production of a virulence factor of the periodontal-disease-causing anaerobic bacterium. J Agric Food Chem. 2004; 52(6):1688-1692. https://doi.org/10.1021/jf0302815.

[176]

Mullish BH, Merrick B, Quraishi MN, et al. The use of faecal microbiota transplant as treatment for recurrent or refractory Clostridioides difficile infection and other potential indications: second edition of Joint British Society of Gastroenterology (BSG) and Healthcare Infection Society (HIS) Guidelines. Gut. 2024; 73(7):1052-1075. https://doi.org/10.1136/gutjnl-2023-331550.

[177]

Moayyedi P, Surette MG, Kim PT, et al. Fecal microbiota transplantation induces remission in patients with active ulcerative colitis in a randomized controlled trial. Gastroenterology. 2015; 149(1):102-109. https://doi.org/10.1053/j.gastro.2015.04.001.

[178]

Caballero-Flores G, Pickard JM, Núñez G, et al. Microbiota-mediated colonization resistance: mechanisms and regulation. Nat Rev Microbiol. 2023; 21(6):347-360. https://doi.org/10.1038/s41579-022-00833-7.

[179]

Cheng XB, Zhao CL, Jin ZW, et al. Natural products: potential therapeutic agents for atherosclerosis. Chin J Nat Med. 2022; 20(11):830-845. https://doi.org/10.1016/S1875-5364(22)60219-X.

[180]

Zhang NN, Jiang ZM, Li SZ, et al. Evolving interplay between natural products and gut microbiota. Eur J Pharmacol. 2023;949:175557. https://doi.org/10.1016/j.ejphar.2023.175557.

[181]

Desai MS, Seekatz AM, Koropatkin NM, et al. A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility. Cell. 2016; 167(5):1339-1353. https://doi.org/10.1016/j.cell.2016.10.043.

[182]

Silva E, Teixeira JA, Pereira MO, et al. Evolving biofilm inhibition and eradication in clinical settings through plant-based antibiofilm agents. Phytomedicine. 2023;119:154973. https://doi.org/10.1016/j.phymed.2023.154973.

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