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线粒体自噬调节肾脏疾病。

Mitophagy Regulates Kidney Diseases.

作者信息

Fan Xiaolu, Wu Linlin, Wang Fengqi, Liu Dong, Cen Xufeng, Xia Hongguang

机构信息

Research Center of Clinical Pharmacy of The First Affiliated Hospital and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.

Hangzhou PhecdaMed Co., Ltd, Hangzhou, China.

出版信息

Kidney Dis (Basel). 2024 Sep 18;10(6):573-587. doi: 10.1159/000541486. eCollection 2024 Dec.

Abstract

BACKGROUND

Mitophagy is a crucial process involved in maintaining cellular homeostasis by selectively eliminating damaged or surplus mitochondria. As the kidney is an organ with a high dynamic metabolic rate and abundant mitochondria, it is particularly crucial to control mitochondrial quality through mitophagy. Dysregulation of mitophagy has been associated with various renal diseases, including acute and chronic kidney diseases, and therefore a better understanding of the links between mitophagy and these diseases may present new opportunities for therapeutic interventions.

SUMMARY

Mitophagy plays a pivotal role in the development of kidney diseases. Upregulation and downregulation of mitophagy have been observed in various kidney diseases, such as renal ischemia-reperfusion injury, contrast-induced acute kidney injury, diabetic nephropathy, kidney fibrosis, and several inherited renal diseases. A growing body of research has suggested that PINK1 and Parkin, the main mitophagy regulatory proteins, represent promising potential therapeutic targets for kidney diseases. In this review, we summarize the latest insights into how the progression of renal diseases can be mitigated through the regulation of mitophagy, while highlighting their performance in clinical trials.

KEY MESSAGE

This review comprehensively outlines the mechanisms of mitophagy and its role in numerous kidney diseases. While early research holds promise, most mitophagy-centered therapeutic approaches have yet to reach the clinical application stage.

摘要

背景

线粒体自噬是一个关键过程,通过选择性清除受损或多余的线粒体来维持细胞内稳态。由于肾脏是一个具有高动态代谢率且富含线粒体的器官,通过线粒体自噬控制线粒体质量尤为重要。线粒体自噬失调与包括急性和慢性肾脏病在内的各种肾脏疾病相关,因此更好地理解线粒体自噬与这些疾病之间的联系可能为治疗干预带来新机会。

总结

线粒体自噬在肾脏疾病的发展中起关键作用。在各种肾脏疾病中,如肾缺血再灌注损伤、造影剂诱导的急性肾损伤、糖尿病肾病、肾纤维化和几种遗传性肾脏疾病,都观察到了线粒体自噬的上调和下调。越来越多的研究表明,主要的线粒体自噬调节蛋白PINK1和Parkin是肾脏疾病有前景的潜在治疗靶点。在本综述中,我们总结了关于如何通过调节线粒体自噬减轻肾脏疾病进展的最新见解,同时强调它们在临床试验中的表现。

关键信息

本综述全面概述了线粒体自噬的机制及其在众多肾脏疾病中的作用。虽然早期研究很有前景,但大多数以线粒体自噬为中心的治疗方法尚未达到临床应用阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772d/11631111/ebd5e35c064d/kdd-2024-0010-0006-541486_F01.jpg

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