title: Cardiac postconditioning.
abstract: In the heart, ischemia/reperfusion damage occurs mainly during the first minutes of reperfusion. Recently, it has been shown that the heart can be protected against the extension of ischemia/reperfusion injury if brief coronary occlusions are performed just at the beginning of the reperfusion. This procedure has been called postconditioning (PostC). It can also be elicited by pharmacological intervention, that is, pharmacological PostC. In particular, PostC limits infarct size, apoptosis, endothelial dysfunction, neutrophil adherence, and arrhythmias. Similar to preconditioning, PostC may trigger signaling pathways, including reperfusion injury salvage kinase and survivor activating factor enhancement pathways. PostC-induced protection also involves intracellular acidosis and early redox-sensitive mechanisms. However, controversies exist on the nature of receptors and main pathway(s) involved in PostC. Protective pathways activated by PostC appear to converge on mitochondria and, in particular, on mitochondrial permeability transition pores. Preliminary clinical data indicate that drugs targeting mitochondrial permeability transition pore or reperfusion injury salvage kinases may confer benefits to patients with acute myocardial infarction above that provided by myocardial reperfusion alone. Future studies must define the principal protective cascades, the interdependence of the signaling pathways, and the optimal pharmacological target and agent(s) for protection. These studies must also consider the possible confounding effects of comorbidities and their drug treatments.
authors: Pasquale
authors: P
authors: Pagliaro
authors: Claudia
authors: C
authors: Penna
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D006321:Heart / Q000503:physiopathology; D006801:Humans; D057775:Ischemic Postconditioning; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D009203:Myocardial Infarction / Q000378:metabolism / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control / Q000628:therapy; D010084:Oxidation-Reduction; D011956:Receptors, Cell Surface / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D011956:Receptors, Cell Surface; D000255:Adenosine Triphosphate