title: Arginase as a target for treatment of myocardial ischemia-reperfusion injury.
abstract: Two distinct enzymes of arginase (1 and 2) are critically regulating nitric oxide (NO) bioavailability by competing with NO synthase for their common substrate l-arginine. Increased expression and activity of arginase is observed in atherosclerosis and myocardial ischemia-reperfusion (I/R). Several studies have demonstrated a key pathophysiological role of increased activity of arginase during I/R. Pharmacological inhibition of arginase results in restoration of NO availability and salvage of myocardium during I/R. Arginase inhibition might be a promising therapeutic strategy for the limitation of myocardial injury in acute myocardial infarction. Current understanding of the role of arginase and efficacy of arginase inhibition during myocardial I/R is reviewed in the present article.
authors.affiliation: Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, S-171 76 Stockholm, Sweden. Electronic address: yahor.tratsiakovich@ki.se.
authors.forename: Yahor
authors.initials: Y
authors.lastname: Tratsiakovich
authors.forename: Jiangning
authors.initials: J
authors.lastname: Yang
authors.forename: Adrian Thomas
authors.initials: AT
authors.lastname: Gonon
authors.forename: Per-Ove
authors.initials: PO
authors.lastname: Sjöquist
authors.forename: John
authors.initials: J
authors.lastname: Pernow
mesh_terms: D000818:Animals; D001119:Arginase / Q000378:metabolism*; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism
chemical_list: D009569:Nitric Oxide; D001119:Arginase
keywords: Arginase; Ischemia-reperfusion; Nitric oxide