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dc.contributor.authorBadalzadeh, R
dc.contributor.authorMokhtari, B
dc.contributor.authorYavari, R
dc.date.accessioned2018-08-26T07:43:19Z
dc.date.available2018-08-26T07:43:19Z
dc.date.issued2015
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/47981
dc.description.abstractIschemic 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.
dc.language.isoEnglish
dc.relation.ispartofJOURNAL OF PHYSIOLOGICAL SCIENCES
dc.subjectMyocardial reperfusion injury
dc.subjectApoptosis
dc.subjectDiabetes
dc.subjectPreconditioning
dc.subjectPostconditioning
dc.titleContribution of apoptosis in myocardial reperfusion injury and loss of cardioprotection in diabetes mellitus
dc.typeReview
dc.citation.volume65
dc.citation.issue3
dc.citation.spage201
dc.citation.epage215
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1007/s12576-015-0365-8


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