Mitochondrial dysfunction in the pathophysiology of renal diseases.

IF 3.4 American journal of physiology. Renal physiology Pub Date : 2024-05-01 Epub Date: 2024-03-07 DOI:10.1152/ajprenal.00189.2023
Yuxian Guo, Ruochen Che, Peipei Wang, Aihua Zhang
{"title":"Mitochondrial dysfunction in the pathophysiology of renal diseases.","authors":"Yuxian Guo, Ruochen Che, Peipei Wang, Aihua Zhang","doi":"10.1152/ajprenal.00189.2023","DOIUrl":null,"url":null,"abstract":"<p><p>Mitochondria are essential organelles in the human body, serving as the metabolic factory of the whole organism. When mitochondria are dysfunctional, it can affect all organs of the body. The kidney is rich in mitochondria, and its function is closely related to the development of kidney diseases. Studying the relationship between mitochondria and kidney disease progression is of great interest. In the past decade, scientists have made inspiring progress in investigating the role of mitochondria in the pathophysiology of renal diseases. This article discusses various mechanisms for maintaining mitochondrial quality, including mitochondrial energetics, mitochondrial biogenesis, mitochondrial dynamics, mitochondrial DNA repair, mitochondrial proteolysis and the unfolded protein response, mitochondrial autophagy, mitochondria-derived vesicles, and mitocytosis. The article also highlights the cross talk between mitochondria and other organelles, with a focus on kidney diseases. Finally, the article concludes with an overview of mitochondria-related clinical research.</p>","PeriodicalId":93867,"journal":{"name":"American journal of physiology. Renal physiology","volume":" ","pages":"F768-F779"},"PeriodicalIF":3.4000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of physiology. Renal physiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1152/ajprenal.00189.2023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/3/7 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Mitochondria are essential organelles in the human body, serving as the metabolic factory of the whole organism. When mitochondria are dysfunctional, it can affect all organs of the body. The kidney is rich in mitochondria, and its function is closely related to the development of kidney diseases. Studying the relationship between mitochondria and kidney disease progression is of great interest. In the past decade, scientists have made inspiring progress in investigating the role of mitochondria in the pathophysiology of renal diseases. This article discusses various mechanisms for maintaining mitochondrial quality, including mitochondrial energetics, mitochondrial biogenesis, mitochondrial dynamics, mitochondrial DNA repair, mitochondrial proteolysis and the unfolded protein response, mitochondrial autophagy, mitochondria-derived vesicles, and mitocytosis. The article also highlights the cross talk between mitochondria and other organelles, with a focus on kidney diseases. Finally, the article concludes with an overview of mitochondria-related clinical research.

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
肾脏疾病病理生理学中的线粒体功能障碍。
线粒体是人体的重要细胞器,是整个机体的新陈代谢工厂。线粒体一旦出现功能障碍,就会影响人体的各个器官。肾脏中含有丰富的线粒体,其功能与肾脏疾病的发生密切相关。研究线粒体与肾脏疾病进展之间的关系非常有意义。近十年来,科学家们在研究线粒体在肾脏疾病病理生理学中的作用方面取得了令人鼓舞的进展。本文讨论了维持线粒体质量的各种机制,包括线粒体能量学、线粒体生物生成、线粒体动力学、线粒体 DNA 修复、线粒体蛋白水解和 UPR、线粒体自噬、线粒体衍生囊泡和有丝分裂。文章还以肾脏疾病为重点,强调了线粒体与其他细胞器之间的相互影响。最后,文章概述了线粒体相关的临床研究。
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
自引率
0.00%
发文量
0
期刊最新文献
Injury-induced Paracrine Effects on the Podocyte's Transcriptome. Kidney kallikrein-1 contributes to cleavage of gamma-ENaC in vivo. Making a portal for podocyte - parietal cell communication in glomerular injury. Vascular transcriptional and metabolic changes precede progressive intra-renal microvascular rarefaction in autosomal dominant polycystic kidney disease. The Transcription Factor TCF21 is Necessary for Adoption of Cell Fates by Foxd1+ Stromal Progenitors during Kidney Development.
×
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