ABSTRACT

Ischemic heart disease is a common cause of morbidity and mortality. The cardiomyocyte is highly dependent on adequate mitochondrial function for its energy supply, and mitochondrial dysfunction is one of the key physiological consequences of ischemia-reperfusion injury. Mitochondrial dysfunction is initiated in the setting of myocardial ischemia, and this dysfunction persists and increases upon reperfusion. The extent of ischemia-reperfusion injury, and thus of mitochondrial injury, is a key determinant of post-ischemic cellular function. Once mitochondria were identified for the integral role they play in the response to ischemic injury, numerous interventions targeting the various mediators of mitochondrial ischemic injury have been hypothesized with little clinical success. Mitochondrial transplantation is a new strategy which aims to replace damaged mitochondria with viable ones. In pre-clinical and clinical trials, this strategy has demonstrated its potential as a therapy for myocardial rescue, and its early success reinforces the importance of mitochondrial function in healthy myocardium.