Nitric oxide synthase in post-ischaemic remodelling: new pathways and mechanisms

The three isoforms of nitric oxide synthase (NOS), spatially confined in specific intracellular compartments in cardiac cells, have distinct roles in the regulation of contractility in pathophysiological situations. Recently, evidence has emerged that implicates NOS in modulating myocardial remodell...

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Bibliographic Details
Published in:Cardiovascular research 2012-05, Vol.94 (2), p.304-315
Main Authors: Manoury, Boris, Montiel, Virginie, Balligand, Jean-Luc
Format: Article
Language:English
Subjects:
Animals
Heart Failure - metabolism
Heart Failure - physiopathology
Humans
Mice
Myocardium - metabolism
Myocardium - pathology
Nitric Oxide - metabolism
Nitric Oxide Synthase - physiology
Signal Transduction
Ventricular Remodeling - physiology
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Summary:The three isoforms of nitric oxide synthase (NOS), spatially confined in specific intracellular compartments in cardiac cells, have distinct roles in the regulation of contractility in pathophysiological situations. Recently, evidence has emerged that implicates NOS in modulating myocardial remodelling during cardiac stress, including after ischaemic insults. As long as they remain in a coupled state the NOS mostly attenuate hypertrophic remodelling through both cGMP-dependent and independent mechanisms. We review the evidence provided from the phenotype of genetic mouse models as well as from in vitro cell experiments dissecting the signalling effectors involved in the NOS-mediated regulation that justify new therapeutic interventions on the NOS-cGMP axis to attenuate the development of heart failure.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvr360