title: Ischemia reperfusion injury, ischemic conditioning and diabetes mellitus.
abstract: 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.
authors.affiliation: Department of Medicine and Institute of Medical Science, University of Toronto, Toronto, Canada; Department of Vascular Surgery and Kidney Transplantation, University of Strasbourg, Strasbourg, France. Electronic address: anne-catherine.lejay@orange.fr.
authors.forename: Anne
authors.initials: A
authors.lastname: Lejay
authors.affiliation: Department of Medicine and Institute of Medical Science, University of Toronto, Toronto, Canada.
authors.forename: Fei
authors.initials: F
authors.lastname: Fang
authors.affiliation: Department of Pathology, University of Toronto, Toronto, Canada.
authors.forename: Rohan
authors.initials: R
authors.lastname: John
authors.affiliation: Department of Medicine and Institute of Medical Science, University of Toronto, Toronto, Canada.
authors.forename: Julie A D
authors.initials: JA
authors.lastname: Van
authors.affiliation: Department of Medicine and Institute of Medical Science, University of Toronto, Toronto, Canada.
authors.forename: Meredith
authors.initials: M
authors.lastname: Barr
authors.affiliation: Department of Vascular Surgery and Kidney Transplantation, University of Strasbourg, Strasbourg, France.
authors.forename: Fabien
authors.initials: F
authors.lastname: Thaveau
authors.affiliation: Department of Vascular Surgery and Kidney Transplantation, University of Strasbourg, Strasbourg, France.
authors.forename: Nabil
authors.initials: N
authors.lastname: Chakfe
authors.affiliation: Department of Physiology, University of Strasbourg, Strasbourg, France.
authors.forename: Bernard
authors.initials: B
authors.lastname: Geny
authors.affiliation: Department of Medicine and Institute of Medical Science, University of Toronto, Toronto, Canada.
authors.forename: James W
authors.initials: JW
authors.lastname: Scholey
mesh_terms: D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D015398:Signal Transduction
chemical_list: D002118:Calcium