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Ischemia-reperfusion injury is a leading cause of death in Western countries. Currently, the only treatment to reduce infact size and to improve the clinical outcome after myocardial ischemia is the rapid restoration of blood flow and the development of reperfusion techniques has strongly reduced the morbidity and mortality in patients. However, the efficacy of this clinical approach is limited because cardiac reperfusion per se give birth to cellular injury. During the last decades, multiple studies demonstrated that the pathological signals induced by ischemia-reperfusion converge towards mitochondria and that most of cell death in the heart is induced by the permeabilization of mitochondrial membranes in the early reperfusion. The search for drugs able to block or to inhibit mitochondrial membrane permeabilization has been the subject of growing interest. It gave birth to several pharmacological approaches to protect from myocardial ischemia-reperfusion injury in experimental models and clinical settings. This review describes these mitochondrial-targeting strategies with a focus on new pharmacological approaches which constitute real hope for the future.