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Eur J Pharmacol. 2013 Nov 15;720(1-3):121-3. doi: 10.1016/j.ejphar.2013.10.040. Epub 2013 Oct 29.

Arginase as a target for treatment of myocardial ischemia-reperfusion injury.

Author information

1
Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, S-171 76 Stockholm, Sweden. Electronic address: yahor.tratsiakovich@ki.se.

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.

KEYWORDS:

Arginase; Ischemia-reperfusion; Nitric oxide

PMID:
24183975
DOI:
10.1016/j.ejphar.2013.10.040
[Indexed for MEDLINE]

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