Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review

Atherosclerosis (AS) is the main cause of cardiovascular disease (CVD) and is characterized by endothelial damage, lipid deposition, and chronic inflammation. Gut microbiota plays an important role in the occurrence and development of AS by regulating host metabolism and immunity. As human mitochond...

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Main Authors: Yujuan Li, Shengjie Yang, Xiao Jin, Dan Li, Jing Lu, Xinyue Wang, Min Wu
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-01-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2023.1082817/full
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author Yujuan Li
Shengjie Yang
Xiao Jin
Dan Li
Jing Lu
Jing Lu
Xinyue Wang
Min Wu
author_facet Yujuan Li
Shengjie Yang
Xiao Jin
Dan Li
Jing Lu
Jing Lu
Xinyue Wang
Min Wu
author_sort Yujuan Li
collection DOAJ
description Atherosclerosis (AS) is the main cause of cardiovascular disease (CVD) and is characterized by endothelial damage, lipid deposition, and chronic inflammation. Gut microbiota plays an important role in the occurrence and development of AS by regulating host metabolism and immunity. As human mitochondria evolved from primordial bacteria have homologous characteristics, they are attacked by microbial pathogens as target organelles, thus contributing to energy metabolism disorders, oxidative stress, and apoptosis. Therefore, mitochondria may be a key mediator of intestinal microbiota disorders and AS aggravation. Microbial metabolites, such as short-chain fatty acids, trimethylamine, hydrogen sulfide, and bile acids, also affect mitochondrial function, including mtDNA mutation, oxidative stress, and mitophagy, promoting low-grade inflammation. This further damages cellular homeostasis and the balance of innate immunity, aggravating AS. Herbal medicines and their monomers can effectively ameliorate the intestinal flora and their metabolites, improve mitochondrial function, and inhibit atherosclerotic plaques. This review focuses on the interaction between gut microbiota and mitochondria in AS and explores a therapeutic strategy for restoring mitochondrial function and intestinal microbiota disorders using herbal medicines, aiming to provide new insights for the prevention and treatment of AS.
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spelling doaj.art-4c070c0b65084c8685cb69d694febb162023-01-17T04:41:46ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122023-01-011410.3389/fphar.2023.10828171082817Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A reviewYujuan Li0Shengjie Yang1Xiao Jin2Dan Li3Jing Lu4Jing Lu5Xinyue Wang6Min Wu7Guang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaGuang’an Men Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaAtherosclerosis (AS) is the main cause of cardiovascular disease (CVD) and is characterized by endothelial damage, lipid deposition, and chronic inflammation. Gut microbiota plays an important role in the occurrence and development of AS by regulating host metabolism and immunity. As human mitochondria evolved from primordial bacteria have homologous characteristics, they are attacked by microbial pathogens as target organelles, thus contributing to energy metabolism disorders, oxidative stress, and apoptosis. Therefore, mitochondria may be a key mediator of intestinal microbiota disorders and AS aggravation. Microbial metabolites, such as short-chain fatty acids, trimethylamine, hydrogen sulfide, and bile acids, also affect mitochondrial function, including mtDNA mutation, oxidative stress, and mitophagy, promoting low-grade inflammation. This further damages cellular homeostasis and the balance of innate immunity, aggravating AS. Herbal medicines and their monomers can effectively ameliorate the intestinal flora and their metabolites, improve mitochondrial function, and inhibit atherosclerotic plaques. This review focuses on the interaction between gut microbiota and mitochondria in AS and explores a therapeutic strategy for restoring mitochondrial function and intestinal microbiota disorders using herbal medicines, aiming to provide new insights for the prevention and treatment of AS.https://www.frontiersin.org/articles/10.3389/fphar.2023.1082817/fullatherosclerosismitochondriagut microbiotametabolismherbal medicine
spellingShingle Yujuan Li
Shengjie Yang
Xiao Jin
Dan Li
Jing Lu
Jing Lu
Xinyue Wang
Min Wu
Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
Frontiers in Pharmacology
atherosclerosis
mitochondria
gut microbiota
metabolism
herbal medicine
title Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
title_full Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
title_fullStr Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
title_full_unstemmed Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
title_short Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review
title_sort mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine a review
topic atherosclerosis
mitochondria
gut microbiota
metabolism
herbal medicine
url https://www.frontiersin.org/articles/10.3389/fphar.2023.1082817/full
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