The Cardioprotection of the Insulin-Mediated PI3K/Akt/mTOR Signaling Pathway

被引:206
作者
Yao, Hong [1 ]
Han, Xiangyang [2 ]
Han, Xiuzhen [1 ]
机构
[1] Shandong Univ, Sch Pharmaceut Sci, Dept Pharmacol, Jinan 250012, Shandong, Peoples R China
[2] Hosp Laiwu Steel Grp, Pharmaceut Preparat Sect, Laiwu 271126, Shandong, Peoples R China
关键词
MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; ISCHEMIA-REPERFUSION INJURY; MITOGEN-ACTIVATED PROTEIN; MOUSE-BRAIN ISCHEMIA; PHOSPHOINOSITIDE; 3-KINASE; OXIDATIVE STRESS; CARDIOMYOCYTE SURVIVAL; TRANSCRIPTION FACTORS; CARDIAC-HYPERTROPHY; GLUCOSE-UPTAKE;
D O I
10.1007/s40256-014-0089-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Apoptosis occurs frequently in myocardial infarction, oxidative stress injury, and ischemia/reperfusion injury, and plays a pivotal role in the development of heart diseases. Inhibition of apoptosis alone does not necessarily lead to meaningful rescue in terms of either cardiomyocyte survival or function. Activation of the PI3K/Akt signaling pathway induced by insulin not only inhibits cardiomyocyte apoptosis but also substantially preserves and even improves regional and overall cardiac function. Insulin can protect cardiomyocytes from apoptosis by regulating a number of signaling molecules, such as eNOS, FOXOs, Bad, GSK-3 beta, mTOR, NDRG2, and Nrf2, through activating PI3K and Akt. This review focuses on the protective mechanisms and targets of insulin identified in the prevention and treatment of myocardial injury.
引用
收藏
页码:433 / 442
页数:10
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