Dysfunctional and Dysregulated Nitric Oxide Synthases in Cardiovascular Disease: Mechanisms and Therapeutic Potential.
NOS inhibitor
cardiovascular disease
endothelial NOS
inducible NOS
neuronal NOS
nitric oxide synthase
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
15 Oct 2023
15 Oct 2023
Historique:
received:
13
09
2023
revised:
11
10
2023
accepted:
13
10
2023
medline:
30
10
2023
pubmed:
28
10
2023
entrez:
28
10
2023
Statut:
epublish
Résumé
Nitric oxide (NO) plays an important and diverse signalling role in the cardiovascular system, contributing to the regulation of vascular tone, endothelial function, myocardial function, haemostasis, and thrombosis, amongst many other roles. NO is synthesised through the nitric oxide synthase (NOS)-dependent L-arginine-NO pathway, as well as the nitrate-nitrite-NO pathway. The three isoforms of NOS, namely neuronal (NOS1), inducible (NOS2), and endothelial (NOS3), have different localisation and functions in the human body, and are consequently thought to have differing pathophysiological roles. Furthermore, as we continue to develop a deepened understanding of the different roles of NOS isoforms in disease, the possibility of therapeutically modulating NOS activity has emerged. Indeed, impaired (or dysfunctional), as well as overactive (or dysregulated) NOS activity are attractive therapeutic targets in cardiovascular disease. This review aims to describe recent advances in elucidating the physiological role of NOS isoforms within the cardiovascular system, as well as mechanisms of dysfunctional and dysregulated NOS in cardiovascular disease. We then discuss the modulation of NO and NOS activity as a target in the development of novel cardiovascular therapeutics.
Identifiants
pubmed: 37894881
pii: ijms242015200
doi: 10.3390/ijms242015200
pmc: PMC10607291
pii:
doi:
Substances chimiques
Nitric Oxide
31C4KY9ESH
Nitric Oxide Synthase Type III
EC 1.14.13.39
Nitric Oxide Synthase
EC 1.14.13.39
Protein Isoforms
0
Nitric Oxide Synthase Type II
EC 1.14.13.39
Nitric Oxide Synthase Type I
EC 1.14.13.39
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Medical Research Council
ID : MR/R017751/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE19542
Pays : United Kingdom
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