2011
DOI: 10.1016/j.clinbiochem.2011.06.003
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Serum levels of arginase I are associated with left ventricular function after myocardial infarction

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Cited by 20 publications
(19 citation statements)
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“…There have been several studies regarding increased arginase activity in humans (19) and in experimental animal models (20,21). Jung et al reported that arginase activity was upregulated during ischemia-reperfusion in mouse myocardial tissue.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…There have been several studies regarding increased arginase activity in humans (19) and in experimental animal models (20,21). Jung et al reported that arginase activity was upregulated during ischemia-reperfusion in mouse myocardial tissue.…”
Section: Discussionmentioning
confidence: 99%
“…In parallel with these findings, increased arginase activity was also shown to contribute to vascular endothelial dysfunction in diabetes (22). Moreover, it was demonstrated that serum arginase I activity was significantly increased and that serum arginine levels were depleted in humans after myocardial infarction (19). These authors demonstrated that arginase expression and activity were upregulated in ischemic myocardium and coronary arterioles following ischemia-reperfusion (19).…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, the induction of NOS arginase has been investigated in the inflammatory cells of asthmatic lungs as pathophysiological evidence that the consumption of L-arginine by arginase may lead to the depletion of NO production and endothelial dysfunction; thus, the enlargement of bronchial smooth muscle associated with airway hyperresponsiveness (68). Furthermore, following catabolism by arginase, arginine is no longer available to NOS; thus, subsequent NO synthesis is diminished (9). …”
Section: Introductionmentioning
confidence: 99%
“…Endothelial nitric oxide synthase (eNOS) enzyme activity and nitric oxide level levels were significantly lower in acute myocardial infarction in presence or absence of macrovascular disease (21). The significant low serum nitric oxide level in patients with acute myocardial infarction could be attributed to increased activity of asymmetric dimethylarginine; an endogenous nitric oxide synthase inhibitor (22). Recently, Cavalca et al (2012) reported non significant changes in asymmetric dimethylarginine but significant increase in symmetric dimethylarginine in NSTEMI (23).…”
Section: Discussionmentioning
confidence: 97%