Mitochondrial Quality Control and Melatonin: A Strategy Against Myocardial Injury

IF 2.8 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Biochemical and Molecular Toxicology Pub Date : 2025-02-26 DOI:10.1002/jbt.70194
Nima Ghavamikia, Faranak Mehrnoosh, Farshad Zare, Payam Ali-khiavi, Ali Sinehsepehr, Yasaman Ghodsi Boushehri, Milad Vahedinezhad, Elham Abdollahi, Ahmed Hjazi, Siamak Aminnezhad, Hossein Saffarfar, Sina Hamzehzadeh, Mehrdad Nourizadeh, Sepideh KarkonShayan
{"title":"Mitochondrial Quality Control and Melatonin: A Strategy Against Myocardial Injury","authors":"Nima Ghavamikia,&nbsp;Faranak Mehrnoosh,&nbsp;Farshad Zare,&nbsp;Payam Ali-khiavi,&nbsp;Ali Sinehsepehr,&nbsp;Yasaman Ghodsi Boushehri,&nbsp;Milad Vahedinezhad,&nbsp;Elham Abdollahi,&nbsp;Ahmed Hjazi,&nbsp;Siamak Aminnezhad,&nbsp;Hossein Saffarfar,&nbsp;Sina Hamzehzadeh,&nbsp;Mehrdad Nourizadeh,&nbsp;Sepideh KarkonShayan","doi":"10.1002/jbt.70194","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Melatonin exhibits various biological functions, including regulation of circadian and endocrine rhythms, anti-inflammatory, and antioxidant effects. Aging and damaged mitochondria are major sources of oxidative stress (OS), and mitochondrial quality control (MQC) is crucial for maintaining normal mitochondrial function. Myocardial ischemia-reperfusion injury is a major complication that can arise during reperfusion therapy for coronary heart disease. However, effective intervention strategies are currently lacking. Mitochondrial dysfunction and OS are considered central mechanisms of myocardial reperfusion injury, with mitochondrial-targeted interventions being a potential treatment direction. Recent studies have shown that melatonin improves mitochondrial structure and function through multiple pathways. This review discusses the mechanisms by which melatonin ameliorates myocardial ischemia-reperfusion injury, focusing on MQC, and explores its potential applications in the prevention and treatment of myocardial ischemia-reperfusion injury.</p>\n </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 3","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biochemical and Molecular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70194","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Melatonin exhibits various biological functions, including regulation of circadian and endocrine rhythms, anti-inflammatory, and antioxidant effects. Aging and damaged mitochondria are major sources of oxidative stress (OS), and mitochondrial quality control (MQC) is crucial for maintaining normal mitochondrial function. Myocardial ischemia-reperfusion injury is a major complication that can arise during reperfusion therapy for coronary heart disease. However, effective intervention strategies are currently lacking. Mitochondrial dysfunction and OS are considered central mechanisms of myocardial reperfusion injury, with mitochondrial-targeted interventions being a potential treatment direction. Recent studies have shown that melatonin improves mitochondrial structure and function through multiple pathways. This review discusses the mechanisms by which melatonin ameliorates myocardial ischemia-reperfusion injury, focusing on MQC, and explores its potential applications in the prevention and treatment of myocardial ischemia-reperfusion injury.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
线粒体质量控制和褪黑素:对抗心肌损伤的策略
褪黑素具有多种生物学功能,包括调节昼夜节律和内分泌节律、抗炎和抗氧化作用。老化和线粒体损伤是氧化应激(OS)的主要来源,而线粒体质量控制(MQC)对于维持线粒体正常功能至关重要。心肌缺血再灌注损伤是冠心病再灌注治疗的主要并发症。然而,目前缺乏有效的干预策略。线粒体功能障碍和OS被认为是心肌再灌注损伤的主要机制,线粒体靶向干预是一个潜在的治疗方向。最近的研究表明,褪黑素通过多种途径改善线粒体结构和功能。本文就褪黑素改善心肌缺血-再灌注损伤的机制进行综述,重点探讨其在心肌缺血-再灌注损伤预防和治疗中的潜在应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
5.80
自引率
2.80%
发文量
277
审稿时长
6-12 weeks
期刊介绍: The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
期刊最新文献
Insights Into the Inhibitory Effect of Ofloxacin on Pepsin Through Peptidomics and Bioinformatics Approaches. Pindolol Mitigates Cancer Cachexia by Modulating Inflammation, Lipolysis, and Muscle Atrophy. Geraniol Mitigates Cytarabine-Induced Hepatotoxicity in Mice via PI3K/AKT-Mediated NRF2 Activation. RETRACTION: Vitamin D3 Exerts a Neuroprotective Effect in Metabolic Syndrome Rats: Role of BDNF/TRKB/Akt/GS3Kβ Pathway. Asiatic Acid Ameliorates Indomethacin-Induced Gastric Ulcers in Rats Through Enhancement of TGF-β1.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1