低氧诱导因子-1／低氧反应元件通路在心肌保护中的研究进展

Advances on the study of hypoxia inducible factor-1/hypoxia response element pathway in myocardial protection

背景低氧诱导因子-1（hypoxia inducible factor-1，HIF-1）是目前公认的在缺氧状态下发挥重要作用的核转录因子，其活化后可介导低氧反应保护作用，在一定程度上能够减轻心肌的缺血／再灌注损伤（ischemic reperfusion injury，I／RI）.目的探究HIF-1/低氧反应元件（hypoxiaresponse element，HRE）通路是如何被激活并发挥心肌保护的作用。内容从HIF—I的概述、调节以及HIF-1／HRE通路的激活机制及其心肌保护作用方面进行综述，并以HIF-1为靶点探究后处理的心肌保护作用的机制，对其在心肌保护作用中与其他关键性的转录因子之间的内在联系作一简要综述。趋向后处理能否激活HIF-1／HRE通路诱导红细胞生成素（erythropoietin，EPO）、血红素加氧酶1（hemeoxygenasel，HO-1）、诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS）和血管内皮生长因子（vascular endothelial growth factor，VEGF）等保护性蛋白的表达，以减轻心肌I／RI，尚需进一步探讨。

Background hypoxia inducible factor-1 （HIF-1） is a nuclear transcription factor that plays an important role in hypoxic state. Its activation could mediate the protection of hypoxia response. In particular, it can alleviate myocardial ischemia/ reperfusion injury （I/RI） in a certain extent. Objective To explore the activation and function of HIF-1/hypoxia response element （HRE）pathway. Content Represent an overview of definition, regulation and activation of the HIF-1/HRE pathway and its mechanism in myocardial protection. The role of H1F-1 during the post-proeessiong of myocardial injury. And with other key transcription factors internal relation in myocardial protection are reviewed. Tend Post-processing can activate HIF-1/HRE pathways and induce erythropoietin（EPO）, hemeoxygenasel （HO-1 ）, inducible nitric oxide synthase （iNOS） and vascular endothelial growth faetor（VEGF） protein expression to against myocardial URI, it remains to be further discussed.