title: Cardioprotection against reperfusion injury: updated mechanisms and strategies.
abstract: Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury. While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G protein-coupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3beta (GSK-3beta), and modulation of mitochondrial permeability transition pore (mPTP) opening. These encouraging laboratory findings may help us develop successful clinical strategies to salvage reperfused myocardium in patients with acute myocardial infarction.
authors.affiliation: Department of Anesthesiology, the University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
authors.forename: Jin-Kun
authors.initials: JK
authors.lastname: Xi
authors.forename: Yuan-Zhe
authors.initials: YZ
authors.lastname: Jin
authors.forename: Xun
authors.initials: X
authors.lastname: Cui
authors.forename: Zhelong
authors.initials: Z
authors.lastname: Xu
mesh_terms: D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D006801:Humans; D033681:Mitochondrial Membrane Transport Proteins / Q000502:physiology; D000083162:Mitochondrial Permeability Transition Pore; D009203:Myocardial Infarction / Q000150:complications; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D038362:Glycogen Synthase Kinase 3