title: Type 2 ryanodine receptor: a novel therapeutic target in myocardial ischemia/reperfusion.
abstract: Cardiac pathologies remain the main cause of mortality worldwide. Among them the most common cause is cardiac ischemia. The rapid reperfusion after coronary occlusion has considerably improved the cardiac outcome, however reperfusion per se has deleterious effect also called reperfusion injuries. Cytosolic calcium overload is now well admitted as an essential pathophysiological mechanism involved in reperfusion injuries although the source and origin of calcium remain to be determined. Recent works have pointed out the potential defect of sarcoplasmic reticulum calcium release channels (ryanodine receptor, RyR) as a primary cause of calcium overload during ischemia-reperfusion. This finding opens new pharmacological perspectives in limiting reperfusion injuries since allosteric modulators able to restore and prevents RyR dysfunction have been developed during the last decade.
authors: U1046 Inserm, Université Montpellier 1, Université Montpellier 2, CHRU Montpellier, F-34295 Montpellier, France.
authors: Jérémy
authors: J
authors: Fauconnier
authors: Stéphanie
authors: S
authors: Roberge
authors: Nathalie
authors: N
authors: Saint
authors: Alain
authors: A
authors: Lacampagne
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D006801:Humans; D008929:Mitochondria, Heart / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D019837:Ryanodine Receptor Calcium Release Channel / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000502:physiology
chemical_list: D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium