Role of Endothelial Cells in Myocardial Ischemia-Reperfusion Injury.
Role of Endothelial Cells in Myocardial Ischemia-Reperfusion Injury.
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DOI：
10.2174/1874120701007010001
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Shiu YT
中科院分区：
文献类型：
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作者：
Singhal AK;Symons JD;Boudina S;Jaishy B;Shiu YT
最大限度地减少心肌缺血再灌注损伤具有广泛的临床意义，并且是心脏手术结果的关键调节因素。 “缺血性损伤”是由于血液供应受限导致供氧与足够强度和/或持续时间的需求之间不匹配而导致细胞坏死，而缺血再灌注损伤是在缺血一段时间后恢复血液供应时发生的，通常与细胞凋亡（即程序性细胞死亡）有关。与血管内皮细胞相比，心肌细胞对缺血性损伤更加敏感，在预防心肌缺血再灌注损伤方面最受关注。关于心肌缺血再灌注损伤的各个方面存在许多综合综述。本综述的目的是探讨血管内皮细胞在心肌缺血再灌注损伤中的作用，并促进这一令人兴奋的临床相关领域的进一步研究。涉及的两个具体领域包括：1）数据表明冠状动脉内皮细胞是缺血再灌注损伤后心肌功能障碍的关键介质； 2) 线粒体通透性转换孔参与缺血再灌注损伤导致的内皮细胞死亡。阐明缺血再灌注导致内皮细胞损伤和/或死亡的细胞信号传导途径是开发临床适用策略的关键组成部分，该策略可以最大限度地减少心肌缺血再灌注损伤。
Minimizing myocardial ischemia-reperfusion injury has broad clinical implications and is a critical mediator of cardiac surgical outcomes. “Ischemic injury” results from a restriction in blood supply leading to a mismatch between oxygen supply and demand of a sufficient intensity and/or duration that leads to cell necrosis, whereas ischemia-reperfusion injury occurs when blood supply is restored after a period of ischemia and is usually associated with apoptosis (i.e. programmed cell death). Compared to vascular endothelial cells, cardiac myocytes are more sensitive to ischemic injury and have received the most attention in preventing myocardial ischemia-reperfusion injury. Many comprehensive reviews exist on various aspects of myocardial ischemia-reperfusion injury. The purpose of this review is to examine the role of vascular endothelial cells in myocardial ischemia-reperfusion injury, and to stimulate further research in this exciting and clinically relevant area. Two specific areas that are addressed include: 1) data suggesting that coronary endothelial cells are critical mediators of myocardial dysfunction after ischemia-reperfusion injury; and 2) the involvement of the mitochondrial permeability transition pore in endothelial cell death as a result of an ischemia-reperfusion insult. Elucidating the cellular signaling pathway(s) that leads to endothelial cell injury and/or death in response to ischemia-reperfusion is a key component to developing clinically applicable strategies that might minimize myocardial ischemia-reperfusion injury.