Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 720, Issue 1-3, Pages 121-123Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2013.10.040
Keywords
Arginase; Ischemia-reperfusion; Nitric oxide
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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. (C) 2013 Elsevier By. All rights reserved.
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