THE ROLE OF THE MITOCHONDRIAL CALCIUM UNIPORTER (MCU) IN THE CARDIAC INJURY INDUCED BY ISCHEMIA AND REPERFUSION

Mitochondrial Ca2+ uptake has been suggested to contribute to the cardiac injury induced by ischemia reperfusion. This notion has been derived from studies using pharmacological approaches due to the lack of information in protein involved in mitochondrial Ca2+ uptake (Ferrari, Di Lisa et al. 1982). The recent identification of the molecular identity of the mitochondrial Ca2+ uniporter (MCU) (De Stefani, Raffaello et al. 2011) allows a genetic approaches. Based on the available notion MCU deletion could be protected against I/R injury , that should be exacerbated by MCU overexpression. The present result provide a more complex picture where by a model increase in mitochondrial Ca2+ elicits cardioprotection that is lost under condition of mitochondrial Ca2+ overload. Neonatal rat ventricular myocytes (NRVMs) overexpressing MCU by adenovirus infection showed a reduction in I/R-induced cell death as compared to wild type (wt) cells (41.82% ±8.37 vs 60.44% ±11.68, p