Integrins and integrin-related proteins in cardiac fibrosis.
Integrins and integrin-related proteins in cardiac fibrosis.
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DOI：
10.1016/j.yjmcc.2015.11.010
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发表时间：
2016-04
影响因子：
5
通讯作者：
Manso AM
中科院分区：
文献类型：
--
作者：
Chen C;Li R;Ross RS;Manso AM
心脏纤维化是心脏损伤后愈合机制的主要组成部分之一，因此可能在一系列病理生理条件下导致收缩和舒张期功能障碍。通常，它可以作为心肌梗死后重塑过程的一部分发生，也可以作为对压力超负荷的反应而发生。整合素是细胞表面受体，在细胞黏附和信号转导中发挥作用。最重要的是，在持续收缩心肌的背景下，它们被认为是机械换能器。它们与包括心脏在内的几个器官的纤维化发展有关。本文将重点介绍整合素和整合素相关蛋白在心脏纤维化中的作用，概述这些蛋白在特定心脏病理的纤维化反应中的作用，讨论整合素发挥作用的一些常见的末端效应因子(血管紧张素II、转化生长因子β1和机械应激)，最后讨论如何操作这一组蛋白质可能导致新的治疗方法，从而证明有助于改变心脏纤维化的有害影响。
Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (Angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis.