Lipid-membrane interactions and the pathogenesis of ischemic damage in the myocardium.
Lipid-membrane interactions and the pathogenesis of ischemic damage in the myocardium.
复制标题
脂质膜相互作用和心肌缺血损伤的发病机制。
DOI：
10.1161/01.res.48.1.1
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发表时间：
1981
影响因子：
20.1
通讯作者：
Messineo,FC
中科院分区：
文献类型：
--
作者：
Katz,AM;Messineo,FC
早在一个多世纪以前，当Virchow提出血浆脂质进入血管壁的运输有助于动脉粥样硬化病变的发展时，人们就提出了脂代谢异常在动脉粥样硬化发病机制中的作用。尽管脂质异常导致冠状动脉闭塞的机制仍不完全清楚，但目前已确定血脂异常是导致缺血性心脏病的一个因素。最近，脂代谢异常被认为与缺血性心脏病发病机制的另一个完全不同的方面有关。大量的证据表明，脂质代谢的改变可以通过改变心肌细胞膜的性质来改变心脏功能，这些功能变化可能导致心肌收缩能力下降，导致心律失常，并最终导致冠状动脉闭塞后的细胞死亡。本文将对其中一些脂质代谢紊乱以及它们可能通过改变缺血心脏的膜功能的可能机制进行综述。
A ROLE for abnormal lipid metabolism in the pathogenesis of atherosclerosis was suggested over a century ago, when Virchow proposed that transport of plasma lipids into the walls of blood vessels contributed to the development of atheromatous lesions. Lipid abnormalities are now firmly established as one factor leading to ischemic heart disease, although the mechanism by which they lead to coronary artery occlusion remains incompletely understood. More recently, abnormalities of lipid metabolism have been implicated in another quite different aspect of the pathogenesis of ischemic heart disease. A large body of evidence now indicates that altered lipid metabolism can alter cardiac function by changing the properties of cardiac cell membranes, and that these functional changes may contribute to the decline in myocardial contractility, the arrhythmias, and the eventual cell death that follow coronary artery occlusion. This article will review some of these disorders in lipid metabolism and possible mechanisms by which they might modify membrane function in the ischemic heart.