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线粒体相关内质网膜(MAMs)的结构与功能及其在心血管疾病中的作用。

Structure and Function of Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Role in Cardiovascular Diseases.

机构信息

Department of Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Department of Physiology and Neurobiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China.

出版信息

Oxid Med Cell Longev. 2021 Jul 11;2021:4578809. doi: 10.1155/2021/4578809. eCollection 2021.

DOI:10.1155/2021/4578809
PMID:34336092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8289621/
Abstract

Abnormal function of suborganelles such as mitochondria and endoplasmic reticulum often leads to abnormal function of cardiomyocytes or vascular endothelial cells and cardiovascular disease (CVD). Mitochondria-associated membrane (MAM) is involved in several important cellular functions. Increasing evidence shows that MAM is involved in the pathogenesis of CVD. MAM mediates multiple cellular processes, including calcium homeostasis regulation, lipid metabolism, unfolded protein response, ROS, mitochondrial dynamics, autophagy, apoptosis, and inflammation, which are key risk factors for CVD. In this review, we discuss the structure of MAM and MAM-associated proteins, their role in CVD progression, and the potential use of MAM as the therapeutic targets for CVD treatment.

摘要

亚细胞器(如线粒体和内质网)的功能异常常导致心肌细胞或血管内皮细胞功能异常和心血管疾病(CVD)。线粒体相关膜(MAM)参与了几种重要的细胞功能。越来越多的证据表明,MAM 参与了 CVD 的发病机制。MAM 介导多种细胞过程,包括钙稳态调节、脂质代谢、未折叠蛋白反应、ROS、线粒体动力学、自噬、细胞凋亡和炎症,这些都是 CVD 的关键危险因素。在这篇综述中,我们讨论了 MAM 的结构及其相关蛋白在 CVD 进展中的作用,以及将 MAM 作为 CVD 治疗的治疗靶点的潜力。

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FASEB Bioadv. 2021 Jan 25;3(3):123-135. doi: 10.1096/fba.2020-00039. eCollection 2021 Mar.
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Cell Rep. 2021 Mar 16;34(11):108873. doi: 10.1016/j.celrep.2021.108873.
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Calcium mitigates fluoride-induced kallikrein 4 inhibition via PERK/eIF2α/ATF4/CHOP endoplasmic reticulum stress pathway in ameloblast-lineage cells.
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Front Cardiovasc Med. 2025 May 30;12:1535401. doi: 10.3389/fcvm.2025.1535401. eCollection 2025.
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