Fiche publication
Date publication
février 2016
Journal
Journal of molecular and cellular cardiology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GENY Bernard
Tous les auteurs :
Lejay A, Fang F, John R, Van JA, Barr M, Thaveau F, Chakfe N, Geny B, Scholey JW
Lien Pubmed
Résumé
Ischemia/reperfusion, which is characterized by deficient oxygen supply and subsequent restoration of blood flow, can cause irreversible damages to tissue. Mechanisms contributing to the pathogenesis of ischemia reperfusion injury are complex, multifactorial and highly integrated. Extensive research has focused on increasing organ tolerance to ischemia reperfusion injury, especially through the use of ischemic conditioning strategies. Of morbidities that potentially compromise the protective mechanisms of the heart, diabetes mellitus appears primarily important to study. Diabetes mellitus increases myocardial susceptibility to ischemia reperfusion injury and also modifies myocardial responses to ischemic conditioning strategies by disruption of intracellular signaling responsible for enhancement of resistance to cell death. The purpose of this review is twofold: first, to summarize mechanisms underlying ischemia reperfusion injury and the signal transduction pathways underlying ischemic conditioning cardioprotection; and second, to focus on diabetes mellitus and mechanisms that may be responsible for the lack of effect of ischemic conditioning strategies in diabetes.
Mots clés
Animals, Apoptosis, Calcium, metabolism, Diabetes Complications, Diabetes Mellitus, metabolism, Endoplasmic Reticulum Stress, Humans, Ischemic Preconditioning, Myocardial, Myocardial Infarction, complications, Myocardial Reperfusion Injury, complications, Myocardium, metabolism, Myocytes, Cardiac, metabolism, Oxidative Stress, Signal Transduction
Référence
J Mol Cell Cardiol. 2016 Feb;91:11-22
