title: Diabetic inhibition of preconditioning- and postconditioning-mediated myocardial protection against ischemia/reperfusion injury.
abstract: Ischemic 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-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β 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-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.
authors.affiliation: The Cardiovascular Center, The First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China.
authors.forename: Xia
authors.initials: X
authors.lastname: Yin
authors.forename: Yang
authors.initials: Y
authors.lastname: Zheng
authors.forename: Xujie
authors.initials: X
authors.lastname: Zhai
authors.forename: Xin
authors.initials: X
authors.lastname: Zhao
authors.forename: Lu
authors.initials: L
authors.lastname: Cai
mesh_terms: D000818:Animals; D048909:Diabetes Complications / Q000201:enzymology / Q000453:epidemiology* / Q000503:physiopathology; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006801:Humans; D057775:Ischemic Postconditioning / Q000706:statistics & numerical data*; D019157:Ischemic Preconditioning, Myocardial / Q000706:statistics & numerical data*; D051379:Mice; D009203:Myocardial Infarction / Q000201:enzymology / Q000453:epidemiology / Q000401:mortality*; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000453:epidemiology*; D009206:Myocardium / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D015398:Signal Transduction
chemical_list: D019869:Phosphatidylinositol 3-Kinases; C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; C000605508:Gsk3b protein, rat; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3