Commentary: Neutral Commentary on Frontiers Article “Cobalt Chloride Upregulates Impaired HIF-1α Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats”

摘要

Coronary heart diseases, including acute myocardial infarction (MI), accounts for high mortality rates in the United States. In addition, diabetes exists as a comorbidity for the majority of all myocardial infarction mortalities (Kannel and McGee, 1979; Danaei et al., 2009) due from occluded coronary circulation, myocardial energy dysregulation, and insulin resistance (Wells et al., 2013). The prognosis and mortality rates from MI depend on the infarction size, which also determines the rate of progression to heart failure (Pfeffer and Braunwald, 1990). Therefore, understanding the molecular signaling cascades that occur in the myocardium due to myocardial infarction is necessary to identify novel therapeutic targets to mitigate the cardiac damage and progression to heart failure. Previous reports have observed the pre- and post-conditioning of sevoflurane upon the heart for protection against ischemia reperfusion (IR) injury involved PI3K-AKT, ERK1/2, and GSK3β signaling pathway (Cadenas et al., 2010). However, more recent studies have focused upon the beneficial effects of Hypoxia inducible factor 1 alpha (HIF-α) cardioprotective signaling mechanism (Hwang et al., 2015; Nanayakkara et al., 2015). Recent studies utilizing an intermittent hypoxia technique in a Hypoxia Inducible Factor-1 (HIF-1α) knockout mouse implicated HIF-1α to be the critical mediator of ischemic pre and post-conditioning (Eckle et al., 2008; Zhao et al., 2010). These reports validate the significance of HIF-1α in conditioning via stabilization of HIF-1α (Zhao et al., 2010). The current manuscript titled,” Cobalt Chloride Upregulates Impaired HIF-1-alpha Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats “ by Wu et al., in the journal Frontiers Physiology, 2017 June 13;8:395, further investigates the scope of HIF-1α signaling in the cardioprotective sevoflurane signaling against IR injury in the diabetic heart (Wu et al., 2017).