C subunit of F1/FO-ATP synthase as target for preventing the detrimental effect of myocardial ischemia/reperfusion injury

Objective: The pathophysiological effects of coronary heart diseases are imputable to the hurtful consequences of ischemia-reperfusion injury (IRI). The opening of a large pore in the mitochondrial membrane, namely, the mitochondrial permeability transition pore (mPTP), is widely recognized as the final step of IRI and is responsible for mitochondrial and cardiomyocyte death. We provided evidences that c subunit of the F1/FO-ATP synthase (FFAS) owns a pivotal role in mPTP formation and activity and thus we sought to test a new mPTP opening inhibitor directed against the c subunit, namely IB13, for the treatment of IRI in ex-vivo model of myocardial infarction.