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心肾综合征中线粒体自噬的分子机制及干预策略

The molecular mechanisms and intervention strategies of mitophagy in cardiorenal syndrome.

作者信息

Yao Mengying, Liu Yong, Sun Mengjia, Qin Shaozong, Xin Wang, Guan Xu, Zhang Bo, He Ting, Huang Yinghui

机构信息

Department of Nephrology, The key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China.

Department of Cardiology, Institute of Cardiovascular Diseases of PLA, The Second Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, China.

出版信息

Front Physiol. 2022 Oct 24;13:1008517. doi: 10.3389/fphys.2022.1008517. eCollection 2022.

DOI:10.3389/fphys.2022.1008517
PMID:36353377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9638141/
Abstract

Cardiorenal syndrome (CRS) is defined as a disorder of the heart and kidney, in which acute or chronic injury of one organ may lead to acute or chronic dysfunction of the other. It is characterized by high morbidity and mortality, resulting in high economic costs and social burdens. However, there is currently no effective drug-based treatment. Emerging evidence implicates the involvement of mitophagy in the progression of CRS, including cardiovascular disease (CVD) and chronic kidney disease (CKD). In this review, we summarized the crucial roles and molecular mechanisms of mitophagy in the pathophysiology of CRS. It has been reported that mitophagy impairment contributes to a vicious loop between CKD and CVD, which ultimately accelerates the progression of CRS. Further, recent studies revealed that targeting mitophagy may serve as a promising therapeutic approach for CRS, including clinical drugs, stem cells and small molecule agents. Therefore, studies focusing on mitophagy may benefit for expanding innovative basic research, clinical trials, and therapeutic strategies for CRS.

摘要

心肾综合征（CRS）被定义为心脏和肾脏的一种紊乱状态，其中一个器官的急性或慢性损伤可能导致另一个器官的急性或慢性功能障碍。其特点是发病率和死亡率高，造成高昂的经济成本和社会负担。然而，目前尚无有效的药物治疗方法。新出现的证据表明，线粒体自噬参与了CRS的进展，包括心血管疾病（CVD）和慢性肾脏病（CKD）。在本综述中，我们总结了线粒体自噬在CRS病理生理学中的关键作用和分子机制。据报道，线粒体自噬功能障碍导致CKD和CVD之间的恶性循环，最终加速CRS的进展。此外，最近的研究表明，靶向线粒体自噬可能是一种有前景的CRS治疗方法，包括临床药物、干细胞和小分子药物。因此，专注于线粒体自噬的研究可能有助于拓展CRS的创新性基础研究、临床试验和治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/7ba7fc5316c9/fphys-13-1008517-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/00877ea7a483/fphys-13-1008517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/3cf17694b379/fphys-13-1008517-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/7ba7fc5316c9/fphys-13-1008517-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/00877ea7a483/fphys-13-1008517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/3cf17694b379/fphys-13-1008517-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b491/9638141/7ba7fc5316c9/fphys-13-1008517-g003.jpg

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