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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.

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。

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