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心肌梗死中线粒体质量控制的机制和治疗进展。

Advances in the mechanism and treatment of mitochondrial quality control involved in myocardial infarction.

机构信息

Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.

出版信息

J Cell Mol Med. 2021 Aug;25(15):7110-7121. doi: 10.1111/jcmm.16744. Epub 2021 Jun 23.

DOI:10.1111/jcmm.16744
PMID:34160885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8335700/
Abstract

Mitochondria are important organelles in eukaryotic cells. Normal mitochondrial homeostasis is subject to a strict mitochondrial quality control system, including the strict regulation of mitochondrial production, fission/fusion and mitophagy. The strict and accurate modulation of the mitochondrial quality control system, comprising the mitochondrial fission/fusion, mitophagy and other processes, can ameliorate the myocardial injury of myocardial ischaemia and ischaemia-reperfusion after myocardial infarction, which plays an important role in myocardial protection after myocardial infarction. Further research into the mechanism will help identify new therapeutic targets and drugs for the treatment of myocardial infarction. This article aims to summarize the recent research regarding the mitochondrial quality control system and its molecular mechanism involved in myocardial infarction, as well as the potential therapeutic targets in the future.

摘要

线粒体是真核细胞中的重要细胞器。正常的线粒体动态平衡受到严格的线粒体质量控制系统的调控,包括线粒体的产生、分裂/融合和自噬的严格调控。线粒体质量控制系统的严格和精确调节,包括线粒体分裂/融合、自噬和其他过程,可以改善心肌缺血和心肌梗死后再灌注引起的心肌损伤,对心肌梗死后的心肌保护起着重要作用。进一步研究其机制有助于确定治疗心肌梗死的新的治疗靶点和药物。本文旨在总结线粒体质量控制系统及其在心肌梗死中的分子机制的最新研究进展,以及未来的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/4fcbdac4a542/JCMM-25-7110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/3d89e2608efd/JCMM-25-7110-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/952c97daf930/JCMM-25-7110-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/17b45f6784bc/JCMM-25-7110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/4fcbdac4a542/JCMM-25-7110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/3d89e2608efd/JCMM-25-7110-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/952c97daf930/JCMM-25-7110-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/17b45f6784bc/JCMM-25-7110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e478/8335700/4fcbdac4a542/JCMM-25-7110-g002.jpg

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Front Cell Dev Biol. 2021 Apr 1;9:636553. doi: 10.3389/fcell.2021.636553. eCollection 2021.
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Oxid Med Cell Longev. 2021 Mar 27;2021:6635955. doi: 10.1155/2021/6635955. eCollection 2021.
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Melatonin Attenuates ox-LDL-Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling.
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