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Diabetic inhibition of preconditioning- and postconditioning-mediated myocardial protection against ischemia/reperfusion injury Yin X; Zheng Y; Zhai X; Zhao X; Cai LExp Diabetes Res 2012[]; 2012 (ä): 198048Ischemic preconditioning (IPC) or postconditioning (Ipost) is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2-6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3beta pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3beta pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3beta pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3beta pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.|Animals[MESH]|Diabetes Complications/enzymology/*epidemiology/physiopathology[MESH]|Glycogen Synthase Kinase 3 beta[MESH]|Glycogen Synthase Kinase 3/metabolism[MESH]|Humans[MESH]|Ischemic Postconditioning/*statistics & numerical data[MESH]|Ischemic Preconditioning, Myocardial/*statistics & numerical data[MESH]|Mice[MESH]|Myocardial Infarction/enzymology/epidemiology/*mortality[MESH]|Myocardial Reperfusion Injury/enzymology/*epidemiology[MESH]|Myocardium/metabolism[MESH]|Phosphatidylinositol 3-Kinases/metabolism[MESH]|Proto-Oncogene Proteins c-akt/metabolism[MESH]|Rats[MESH]|Signal Transduction[MESH] |
