During myocardial ischemia/reperfusion, mitochondria are both a source and a target of injury. In cardioprotective maneuvers such as ischemic and pharmacological pre- and postconditioning mitochondria have a decisive role. Since about 99% of the mitochondrial proteins are encoded in the nucleus, deleterious and protective mitochondrial effects most likely comprise the import of cytosolic proteins. The present review therefore discusses the role of mitochondria in myocardial ischemia/reperfusion injury and protection from it, focusing on some cytosolic proteins, which are translocated into mitochondria before, during, or following ischemia/reperfusion. Both morphological and functional alterations are discussed at the level of the heart, the cardiomyocyte and/or the mitochondrion itself. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.
Research Highlights
► Mitochondria are both source and target of myocardial ischemia/reperfusion injury. ► Nuclear-encoded proteins are imported into mitochondria. ► Nuclear-encoded proteins affect mitochondrial morphology and function.
