Peng Liu, Zhen-Yu Liu, Sui Mao, Xin-Yu Shen, Zhi-Yan Liu, Li-Chan Lin, Jing-Jing Yang, Ye Zhang, Jian-Yuan Zhao, Hui Tao
{"title":"Targeted mitochondrial function for cardiac fibrosis: An epigenetic perspective.","authors":"Peng Liu, Zhen-Yu Liu, Sui Mao, Xin-Yu Shen, Zhi-Yan Liu, Li-Chan Lin, Jing-Jing Yang, Ye Zhang, Jian-Yuan Zhao, Hui Tao","doi":"10.1016/j.freeradbiomed.2025.01.001","DOIUrl":null,"url":null,"abstract":"<p><p>Mitochondria, commonly referred to as \"energy factories\"of cells, play a crucial role in the function and survival of cardiomyocytes. However, as research on cardiac fibrosis has advanced, mitochondrial dysfunction(including changes in energy metabolism, calcium ion imbalance, increased oxidative stress, and apoptosis)is now recognized as a significant pathophysiological pathway involved in cardiac remodeling and progression, which also negatively affects the function and structure of the heart. In recent years, research focusing on targeting mitochondria has gained significant attention, offering new approaches for treating cardiac fibrosis. Targeted mitochondrial therapy for cardiac fibrosis represents an emerging therapeutic strategy that aims to inhibit cardiac fibroblast proliferation or protect cardiomyocytes from damage by enhancing mitochondrial function. However, current research on epigenetic treatments for cardiac fibrosis through mitochondrial targeting remains limited. This review explores the relationship between mitochondrial dysfunction and cardiac fibrosis, as well as the epigenetic regulatory mechanisms involved in targeted mitochondrial therapy for cardiac fibrosis.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":"163-172"},"PeriodicalIF":7.1000,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Free Radical Biology and Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.freeradbiomed.2025.01.001","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Mitochondria, commonly referred to as "energy factories"of cells, play a crucial role in the function and survival of cardiomyocytes. However, as research on cardiac fibrosis has advanced, mitochondrial dysfunction(including changes in energy metabolism, calcium ion imbalance, increased oxidative stress, and apoptosis)is now recognized as a significant pathophysiological pathway involved in cardiac remodeling and progression, which also negatively affects the function and structure of the heart. In recent years, research focusing on targeting mitochondria has gained significant attention, offering new approaches for treating cardiac fibrosis. Targeted mitochondrial therapy for cardiac fibrosis represents an emerging therapeutic strategy that aims to inhibit cardiac fibroblast proliferation or protect cardiomyocytes from damage by enhancing mitochondrial function. However, current research on epigenetic treatments for cardiac fibrosis through mitochondrial targeting remains limited. This review explores the relationship between mitochondrial dysfunction and cardiac fibrosis, as well as the epigenetic regulatory mechanisms involved in targeted mitochondrial therapy for cardiac fibrosis.
期刊介绍:
Free Radical Biology and Medicine is a leading journal in the field of redox biology, which is the study of the role of reactive oxygen species (ROS) and other oxidizing agents in biological systems. The journal serves as a premier forum for publishing innovative and groundbreaking research that explores the redox biology of health and disease, covering a wide range of topics and disciplines. Free Radical Biology and Medicine also commissions Special Issues that highlight recent advances in both basic and clinical research, with a particular emphasis on the mechanisms underlying altered metabolism and redox signaling. These Special Issues aim to provide a focused platform for the latest research in the field, fostering collaboration and knowledge exchange among researchers and clinicians.