Programmed death as a therapeutic target to reduce myocardial infarction.
Programmed death as a therapeutic target to reduce myocardial infarction.
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DOI：
10.1016/j.tips.2007.07.004
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发表时间：
2007-09
影响因子：
13.8
通讯作者：
K. Webster
中科院分区：
文献类型：
--
作者：
K. Webster
在美国，每年约有200万患者接受血管成形术或搭桥手术来去除冠状动脉闭塞。尽管再灌注对于挽救缺血心肌至关重要，但它也通过激活原缺血组织中的程序性细胞死亡来促进梗死。当线粒体的氧化应激和钙积累导致所谓的线粒体死亡通道激活时，再灌注损伤就开始了。这些通道已成为保护心脏免受梗死的发展策略的焦点。临床前和初步临床研究表明，不同作用方式的药物可使梗死面积减少50%或更多，并显著保护心肌功能。这篇文章回顾了最先进的药理学方法，因为它们能够通过抑制线粒体死亡途径来减少梗死面积。
In the United States, angioplasty or bypass surgery to remove coronary occlusions is performed on approximately two million patients each year. Although reperfusion is essential for salvaging ischemic myocardium, it also promotes infarction by activating programmed cell death in the formerly ischemic tissue. Reperfusion injury begins when oxidative stress and calcium accumulation by the mitochondria cause activation of the so-called mitochondrial death channels. These channels have become the focus of evolving strategies to protect the heart from infarction. Preclinical and preliminary clinical studies indicate that agents with diverse modes of action can reduce infarct size by 50% or more and significantly preserve myocardial functions. This article reviews the most advanced pharmacological approaches for their ability to reduce infarct size by inhibiting the mitochondrial death pathways.