心肌胰岛素抵抗和雷帕霉素靶蛋白信号调控的研究进展  

Cardiac Insulin Resistance and Mammalian Target for Rapamycin Signaling Pathway

作　　者：杨玉桥 钱金桥[1] 

机构地区：[1]昆明医科大学第一附属医院麻醉科,昆明650000

出　　处：《医学综述》2015年第4期579-582,共4页Medical Recapitulate

基　　金：国家自然科学基金(81160035)

摘　　要：心肌胰岛素抵抗是一种与营养过剩和心肾代谢综合征有关的代谢异常。营养过剩能激活肾素-血管紧张素-醛固酮系统,引起循环中增多的营养素、胰岛素和血管紧张素Ⅱ长期暴露于心血管组织中,并通过激活心肌组织中的哺乳动物雷帕霉素靶蛋白(m TOR)/p70S6Kinase1(S6K1)信号通路引起心肌胰岛素抵抗。而最新的研究表明,心肌组织中m TOR信号的激活与适应性心肌肥厚有关,同时还参与形成m TORAT2R信号环路,反馈调控过量激活的m TOR信号,介导心脏保护作用。该文就心肌胰岛素抵抗与m TOR信号调控的研究进展予以综述。Cardiac insulin resistance is a metabolic and function disorder often associated with overnutrition and cardiorenal metabolic syndrome（ CRS）. Overnutrition induces activation of rennin angiotensin aldosterone system（ RAAS） and results in chronic exposure of increased nutrients,insulin and angiotensinⅡ（ AngⅡ） in cardiovascular tissues and circulation,which can mediate activation of mammalian target of rapamycin（ m TOR） /p70S6 kinase/（ S6K1） signaling and cause insulin resistance. Recent studies indicate that the activation of m TOR is involved in adaptive hypertrophy and also exerts cardioprotection effect via forming m TOR AT2 R signaling loop which can balance the enhanced m TOR signaling in cardiac tissue in conditions of overnutrition- induced insulin resistance. Here is to make a review of the research progress in cardiac insulin resistance and m TOR signaling regulation.

关 键 词：营养过剩 胰岛素抵抗 雷帕霉素靶蛋白信号通路 

分 类 号：R542.2[医药卫生—心血管疾病]