Brief episodes of ischemia and reperfusion given before prolonged ischemia protect the myocardium, a
phenomenon referred to as ischemic preconditioning(IPC). Although effective, IPC requires access to
the coronary vessels which is not feasible in the majority of cases. Subsequently, attention has focused on
modifying events occurring at the time of myocardial reperfusion (i.e., ischemic postconditioning, IPostC).
IPC and IPostC activate similar protective mechanisms in the heart. As IPC, IPostC protection depends on
the activation of the survival kinases [phosphatidylinositol 3-kinase (PI3K)?Akt. However, the Reperfusion
Injury Salvage Kinase (RISK) pathway (e.g., PI3K-Akt signaling and especially the newly identified Survivor
Activating Factor Enhancement (SAFE) pathway (i.e., JAK/STAT-3 signaling, which has been shown to be
essential for IPostC to confer cardioprotection and can be activated independently of the RISK pathway
are impaired in the diabetic myocardium, making it less feasible if not impossible to pre or postcondition
diabetic hearts. Research efforts are being made to identify yherapeutic strategies that can resume the RISK
and/or SAFE pathways in order to restore the sensitivity of diabetic heart to IPC and/or IPostC.
Zhengyuan Xia had served as a cardiovascular anesthetist for more than 10 years in China before he completed
his Ph.D study at the University of British Columbia (UBC), in Canada in 2004 and postdoctoral studies at UBC and
University of Calgary in 2007. He is Assistant Professor and Honorary Associate Professor at the University of Hong
Kong and his major focus of research is cardiac protection during ischemia-reperfusion in diabetes. He has published
more than 65 papers in reputed journals and serving as an editorial board member of Journal of Diabetes & Metabolism.
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