title: Mitochondria in postconditioning.
abstract: Several signal transduction pathways are activated by cardioprotective stimuli, including ischemic or pharmacological postconditioning. These pathways converge on a common target, the mitochondria, and cardioprotection by postconditioning is associated with preserved mitochondrial function after ischemia/reperfusion. The present review discusses the role of mitochondria in cardioprotection, especially the involvement of ATP-dependent potassium channels, reactive oxygen species, and the mitochondrial permeability transition pore, and focuses on the effects of postconditioning on mitochondrial function (i.e., their oxygen consumption and calcium retention capacity). The contribution of mitochondria to loss of protection by postconditioning in diseased or aged myocardium is also addressed.
authors.affiliation: Institut für Pathophysiologie, Universitätsklinikum Essen, Hufelandstrasse 55, Essen, Germany. Kerstin.boengler@uk-essen.de
authors.forename: Kerstin
authors.initials: K
authors.lastname: Boengler
authors.forename: Gerd
authors.initials: G
authors.lastname: Heusch
authors.forename: Rainer
authors.initials: R
authors.lastname: Schulz
mesh_terms: D000818:Animals; D006801:Humans; D057775:Ischemic Postconditioning; D019157:Ischemic Preconditioning, Myocardial; D008928:Mitochondria / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism; D015398:Signal Transduction