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心血管疾病中的自噬与氧化应激

Autophagy and oxidative stress in cardiovascular diseases.

作者信息

Mei Yu, Thompson Melissa D, Cohen Richard A, Tong XiaoYong

机构信息

Vascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.

Vascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.

出版信息

Biochim Biophys Acta. 2015 Feb;1852(2):243-51. doi: 10.1016/j.bbadis.2014.05.005. Epub 2014 May 13.

DOI:10.1016/j.bbadis.2014.05.005
PMID:24834848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4231019/
Abstract

Autophagy is a highly conserved degradation process by which intracellular components, including soluble macromolecules (e.g. nucleic acids, proteins, carbohydrates, and lipids) and dysfunctional organelles (e.g. mitochondria, ribosomes, peroxisomes, and endoplasmic reticulum) are degraded by the lysosome. Autophagy is orchestrated by the autophagy related protein (Atg) composed protein complexes to form autophagosomes, which fuse with lysosomes to generate autolysosomes where the contents are degraded to provide energy for cell survival in response to environmental and cellular stress. Autophagy is an important player in cardiovascular disease development such as atherosclerosis, cardiac ischemia/reperfusion, cardiomyopathy, heart failure and hypertension. Autophagy in particular contributes to cardiac ischemia, hypertension and diabetes by interaction with reactive oxygen species generated in endoplasmic reticulum and mitochondria. This review highlights the dual role of autophagy in cardiovascular disease development. Full recognition of autophagy as an adaptive or maladaptive response would provide potential new strategies for cardiovascular disease prevention and management. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.

摘要

自噬是一种高度保守的降解过程,通过该过程,细胞内成分,包括可溶性大分子(如核酸、蛋白质、碳水化合物和脂质)和功能失调的细胞器(如线粒体、核糖体、过氧化物酶体和内质网)被溶酶体降解。自噬由自噬相关蛋白(Atg)组成的蛋白复合物协调,形成自噬体,自噬体与溶酶体融合产生自溶酶体,其中的内容物被降解,以在响应环境和细胞应激时为细胞存活提供能量。自噬在心血管疾病发展过程中发挥重要作用,如动脉粥样硬化、心脏缺血/再灌注、心肌病、心力衰竭和高血压。自噬尤其通过与内质网和线粒体中产生的活性氧相互作用,导致心脏缺血、高血压和糖尿病。本综述强调了自噬在心血管疾病发展中的双重作用。充分认识自噬是一种适应性或适应不良的反应,将为心血管疾病的预防和管理提供潜在的新策略。本文是名为:心血管代谢疾病中的自噬和蛋白质质量控制的特刊的一部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/4231019/6763a748ad06/nihms597215f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/4231019/6763a748ad06/nihms597215f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f0/4231019/6763a748ad06/nihms597215f1.jpg

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Targeting autophagy for the therapeutic application of histone deacetylase inhibitors in ischemia/reperfusion heart injury.
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Antioxidants: a comprehensive review.抗氧化剂:全面综述。
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