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内皮功能障碍作为内皮细胞-心肌细胞通讯障碍的枢纽。

Endothelial dysfunction as a nexus for endothelial cell-cardiomyocyte miscommunication.

机构信息

Division of Cardiology, Johns Hopkins University School of Medicine Baltimore, MD, USA.

Department of Medicine - Cardiovascular, Institute of Molecular Cardiology, and Diabetes and Obesity Center, School of Medicine, University of Louisville Louisville, KY, USA.

出版信息

Front Physiol. 2014 Aug 26;5:328. doi: 10.3389/fphys.2014.00328. eCollection 2014.

DOI:10.3389/fphys.2014.00328
PMID:25206341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4144117/
Abstract

Most studies of the heart focus on cardiomyocytes (CM) at the exclusion of other cell types such as myocardial endothelial cells (EC). Such mono-cellular approaches propagate the presumption that EC provide a mere "passive lining" or supportive role. In fact, EC contribute to a dynamic network regulating vascular tone, cardiac development, and repair. Two distinct EC types, vascular EC and epicardial EC, possess important structural and signaling properties within both the healthy and diseased myocardium. In this review, we address EC-CM interactions in mature, healthy myocardium, followed by a discussion of diseases characterized by EC dysfunction. Finally, we consider strategies to reverse EC-CM "miscommunication" to improve patients' outcomes in various cardiovascular diseases.

摘要

大多数心脏研究都集中在心肌细胞(CM)上,而排除了心肌内皮细胞(EC)等其他细胞类型。这种单一细胞的方法传播了这样一种假设,即 EC 只提供了一种“被动衬里”或支持作用。事实上,EC 有助于形成一个动态的网络,调节血管张力、心脏发育和修复。两种不同的 EC 类型,血管 EC 和心外膜 EC,在健康和患病的心肌中都具有重要的结构和信号特性。在这篇综述中,我们首先讨论了成熟、健康心肌中的 EC-CM 相互作用,然后讨论了以 EC 功能障碍为特征的疾病。最后,我们考虑了逆转 EC-CM“通信错误”的策略,以改善各种心血管疾病患者的预后。

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