Ischemic preconditioning: from molecular mechanisms to therapeutic opportunities.
Ischemic preconditioning: from molecular mechanisms to therapeutic opportunities.
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DOI：
10.1089/ars.2007.1679
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发表时间：
2008-02
影响因子：
6.6
通讯作者：
H. Otani
中科院分区：
文献类型：
--
作者：
H. Otani
缺血/再灌注（I/R）损伤是心功能障碍和梗死面积决定急性心肌梗死后患者预后的主要因素。利用心脏的内源性能力来抵抗I/R损伤，被称为缺血预处理（IPC），已经引起了相当大的兴趣。IPC研究有助于在分子和细胞基础上揭示I/R损伤的病理生理学，并发明潜在的治疗方法来对抗这种损伤。然而，从IPC学到的基础研究成果转化为临床实践往往是不够的，因为大多数基础研究成果来自年轻和健康的动物。IPC的成功实施很少发生在病变心脏中，而病变心脏是激活心脏保护机制以限制心功能障碍和梗死面积的可行疗法的主要目标。因此，本综述的第一个目的是促进理解I/R损伤的病理生理学和IPC在正常心脏中提供的心脏保护机制。然后，我重点讨论了在患病心脏中成功地将IPC从实验室转移到床边的问题和机会。
Ischemia/reperfusion (I/R) injury is a major contributory factor to cardiac dysfunction and infarct size that determines patient prognosis after acute myocardial infarction. Considerable interest exists in harnessing the heart's endogenous capacity to resist I/R injury, known as ischemic preconditioning (IPC). The IPC research has contributed to uncovering the pathophysiology of I/R injury on a molecular and cellular basis and to invent potential therapeutic means to combat such damage. However, the translation of basic research findings learned from IPC into clinical practice has often been inadequate because the majority of basic research findings have stemmed from young and healthy animals. Few if any successful implementations of IPC have occurred in the diseased hearts that are the primary target of viable therapies activating cardioprotective mechanisms to limit cardiac dysfunction and infarct size. Therefore, the first purpose of this review is to facilitate understanding of pathophysiology of I/R injury and the mechanisms of cardioprotection afforded by IPC in the normal heart. Then I focus on the problems and opportunities for successful bench-to-bedside translation of IPC in the diseased hearts.