现有的证据显示，糖尿病心肌缺血/再灌注损伤（ischemia/reperfusion injury, I/RI）较非糖尿病损伤加重，但是其详细的分子机制尚不完全清楚。虽然尚需进一步研究，但是自噬及其相关磷脂酰肌醇-3-激酶-蛋白激酶B-雷帕霉素靶蛋白（phosphatidylinositol-3?-kinase-protein kinase B-mammalian target of rapamycin, PI3K-Akt-mTOR）信号转导通路在糖尿病心肌I/RI过程中发挥的作用越来越受到关注，将来可能成为防治糖尿病心肌I/RI的重要靶点。文章回顾自噬及其相关PI3K?-Akt-mTOR信号转导通路与糖尿病I/RI的关系，重点综述自噬及其相关的PI3K-Akt-mTOR信号转导通路在糖尿病心肌I/RI和缺血预处理心肌保护中的地位和发挥的调节作用。
Available evidences show that myocardial ischemia/reperfusion injury (I/RI) is aggravated in diabetic condition compared with those I/RI happened on non-diabetic condition, but detailed molecular mechanism is not fully understood. Although further investigation is needed, the effects of autophagy and phosphatidylinositol-3-kinase-protein kinase B-mammalian target of rapamycin(PI3K-Akt-mTOR) signaling transduction pathway in diabetic myocardial I/RI have attracted more attention. It may be an important target for prevention of diabetic myocardial I/RI in the future. The aim of this article is to review relationship of autophagy and PI3K-Akt-mTOR signaling transduction pathway with I/RI happened in diabetes mellitus. This article mainly focuses on the role and regulation of autophagy and PI3K-Akt-mTOR signaling transduction pathway in diabetic myocardial I/RI and cardiac-protection of ischemia preconditioning.
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