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本文引用的文献

1
mTORC1 phosphorylates the ULK1-mAtg13-FIP200 autophagy regulatory complex.mTORC1使ULK1-mAtg13-FIP200自噬调节复合物发生磷酸化。
Sci Signal. 2009 Aug 18;2(84):pe51. doi: 10.1126/scisignal.284pe51.
2
Atg32 is a mitochondrial protein that confers selectivity during mitophagy.Atg32是一种在线粒体自噬过程中赋予选择性的线粒体蛋白。
Dev Cell. 2009 Jul;17(1):98-109. doi: 10.1016/j.devcel.2009.06.014.
3
Angiotensin II type 2 receptor antagonizes angiotensin II type 1 receptor-mediated cardiomyocyte autophagy.血管紧张素II 2型受体拮抗血管紧张素II 1型受体介导的心肌细胞自噬。
Hypertension. 2009 Jun;53(6):1032-40. doi: 10.1161/HYPERTENSIONAHA.108.128488. Epub 2009 May 11.
4
Evidence for cardiomyocyte renewal in humans.人类心肌细胞更新的证据。
Science. 2009 Apr 3;324(5923):98-102. doi: 10.1126/science.1164680.
5
Functional significance and morphological characterization of starvation-induced autophagy in the adult heart.成年心脏中饥饿诱导自噬的功能意义及形态学特征
Am J Pathol. 2009 May;174(5):1705-14. doi: 10.2353/ajpath.2009.080875. Epub 2009 Mar 26.
6
Clinical outcome and phenotypic expression in LAMP2 cardiomyopathy.LAMP2 型心肌病的临床结局与表型表达
JAMA. 2009 Mar 25;301(12):1253-9. doi: 10.1001/jama.2009.371.
7
Autophagy is required for preconditioning by the adenosine A1 receptor-selective agonist CCPA.腺苷A1受体选择性激动剂CCPA进行预处理需要自噬。
Basic Res Cardiol. 2009 Mar;104(2):157-67. doi: 10.1007/s00395-009-0006-6. Epub 2009 Feb 26.
8
Autophagy in ischemic heart disease.缺血性心脏病中的自噬
Circ Res. 2009 Jan 30;104(2):150-8. doi: 10.1161/CIRCRESAHA.108.187427.
9
Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.《2009年心脏病和中风统计数据更新:美国心脏协会统计委员会及中风统计小组委员会报告》
Circulation. 2009 Jan 27;119(3):480-6. doi: 10.1161/CIRCULATIONAHA.108.191259.
10
Autophagy in load-induced heart disease.负荷诱导性心脏病中的自噬
Circ Res. 2008 Dec 5;103(12):1363-9. doi: 10.1161/CIRCRESAHA.108.186551.

高血压性心脏病中的自噬作用。

Autophagy in hypertensive heart disease.

机构信息

Department of Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, Texas 75390-8573, USA.

出版信息

J Biol Chem. 2010 Mar 19;285(12):8509-14. doi: 10.1074/jbc.R109.025023. Epub 2010 Jan 29.

DOI:10.1074/jbc.R109.025023
PMID:20118246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2838272/
Abstract

In response to hypertension, the heart manifests robust hypertrophic growth, which offsets load-induced elevations in wall stress. If sustained, this hypertrophic response is a major risk factor for systolic dysfunction and heart failure. Extensive research efforts have focused on the progression from hypertrophy to failure; however, precise understanding of underlying mechanisms remains elusive. Recently, autophagy, a process of cellular cannibalization, has been implicated. Autophagy is activated during ventricular hypertrophy, serving to maintain cellular homeostasis. Excessive autophagy eliminates, however, essential cellular elements and possibly provokes cell death, which together contribute to hypertension-related heart disease.

摘要

针对高血压,心脏会表现出强大的肥厚性生长,以抵消壁应力引起的负荷升高。如果这种肥厚性反应持续存在,它将成为收缩功能障碍和心力衰竭的主要危险因素。大量的研究工作集中在从肥厚到衰竭的进展上;然而,对潜在机制的确切理解仍然难以捉摸。最近,细胞自噬过程已被牵涉其中。自噬在心室肥厚期间被激活,以维持细胞内环境稳定。然而,过度的自噬会消除必要的细胞成分,并可能引发细胞死亡,这两者共同导致与高血压相关的心脏病。