Contribution of apoptosis in myocardial reperfusion injury and loss of cardioprotection in diabetes mellitus.
Ischemic heart disease is one of the major causes of death worldwide. Ischemia is a condition in which blood flow of the myocardium declines, leading to cardiomyocyte death. However, reperfusion of ischemic regions decreases the rate of mortality, but it can also cause later complications. In a clinical setting, ischemic heart disease is always coincident with other co-morbidities such as diabetes. The risk of heart disease increases 2-3 times in diabetic patients. Apoptosis is considered to be one of the main pathophysiological mechanisms of myocardial ischemia-reperfusion injury. Diabetes can disrupt the anti-apoptotic intracellular signaling cascades involved in myocardial protection. Therefore, targeting these changes may be an effective cardioprotective approach in the diabetic myocardium against ischemia-reperfusion injury. In this article, we review the interaction of diabetes with the pathophysiology of myocardial ischemia-reperfusion injury, focusing on the contribution of apoptosis in this context, and then discuss the alterations of pro-apoptotic or anti-apoptotic pathways probably responsible for the loss of cardioprotection in diabetes.
Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran, badalzadehr@tbzmed.ac.ir.
Reza
R
Badalzadeh
Behnaz
B
Mokhtari
Raana
R
Yavari
D017209:Apoptosis; D048909:Diabetes Complications / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007333:Insulin Resistance; D057775:Ischemic Postconditioning; D019157:Ischemic Preconditioning, Myocardial; D054086:KATP Channels / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000150:complications / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D015398:Signal Transduction
D054086:KATP Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore