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急性心肌梗死是目前严重威胁人类健康的致死疾病之一,及时再灌注是限制心肌梗死面积的最有效方法,然而,再灌注本身会导致进一步的心肌损伤。线粒体乙醛脱氢酶(mitochondrial aldehyde dehydrogenase,ALDH2)被广泛熟知为代谢乙醛的酶。越来越多的证据表明ALDH2在心肌缺血再灌注中起到心肌保护的作用。动物实验表明ALDH2可减少心肌梗死面积,减轻心功能紊乱,防止再灌注性心律失常的发生。突变型ALDH2*2基因编码的ALDH2酶活性显著降低,而该基因的突变率在亚洲人群中约为40%。在亚洲人中的流行病学调查表明,ALDH2基因多态性与急性心肌梗死面积和冠状动脉疾病发生率紧密相关。因此,将ALDH2作为治疗心肌缺血再灌注损伤的靶点将很有前景。本文综述ALDH2对缺血再灌注心肌的保护作用及机制,并探讨ALDH2的转化应用研究前景。
Acute myocardial infarction (AMI) is one of the most lethal diseases that currently threaten human health. Timely reperfusion is the most effective way to limit infarct size. However, reperfusion itself can lead to further myocardial damage. Mitochondrial aldehyde dehydrogenase (ALDH2) is widely known as an enzyme that metabolizes acetaldehyde. There is growing evidence that ALDH2 plays a role in myocardial protection during myocardial ischemia-reperfusion. Animal experiments show that ALDH2 can reduce the area of myocardial infarction, reduce cardiac dysfunction and prevent the occurrence of reperfusion arrhythmia. The mutant ALDH2 * 2 gene encodes a significantly reduced ALDH2 enzyme activity, and the mutation rate of this gene is about 40% in the Asian population. Epidemiological studies in Asians indicate that ALDH2 gene polymorphisms are closely related to the area of acute myocardial infarction and the incidence of coronary artery disease. Therefore, the ALDH2 as a target for treatment of myocardial ischemia-reperfusion injury will be very promising. This article reviews the protective effect of ALDH2 on myocardial ischemia-reperfusion and its mechanism, and explores the application prospects of ALDH2 transformation.