The regulation of cardiac intermediary metabolism by NADPH oxidases.
Cardiac metabolism
Intermediary metabolism
NADPH oxidases
Redox signalling
Journal
Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427
Informations de publication
Date de publication:
18 01 2023
18 01 2023
Historique:
received:
01
10
2021
revised:
24
12
2021
accepted:
18
01
2022
pubmed:
25
3
2022
medline:
21
1
2023
entrez:
24
3
2022
Statut:
ppublish
Résumé
NADPH oxidases (NOXs), enzymes whose primary function is to generate reactive oxygen species, are important regulators of the heart's physiological function and response to pathological insults. The role of NOX-driven redox signalling in pathophysiological myocardial remodelling, including processes such as interstitial fibrosis, contractile dysfunction, cellular hypertrophy, and cell survival, is well recognized. While the NOX2 isoform promotes many detrimental effects, the NOX4 isoform has attracted considerable attention as a driver of adaptive stress responses both during pathology and under physiological states such as exercise. Recent studies have begun to define some of the NOX4-modulated mechanisms that may underlie these adaptive responses. In particular, novel functions of NOX4 in driving cellular metabolic changes have emerged. Alterations in cellular metabolism are a recognized hallmark of the heart's response to physiological and pathological stresses. In this review, we highlight the emerging roles of NOX enzymes as important modulators of cellular intermediary metabolism in the heart, linking stress responses not only to myocardial energetics but also other functions. The novel interplay of NOX-modulated redox signalling pathways and intermediary metabolism in the heart is unravelling a new aspect of the fascinating biology of these enzymes which will inform a better understanding of how they drive adaptive responses. We also discuss the implications of these new findings for therapeutic approaches that target metabolism in cardiac disease.
Identifiants
pubmed: 35325070
pii: 6553925
doi: 10.1093/cvr/cvac030
pmc: PMC9847558
doi:
Substances chimiques
NADPH Oxidases
EC 1.6.3.-
Reactive Oxygen Species
0
Protein Isoforms
0
NADPH Oxidase 4
EC 1.6.3.-
Types de publication
Review
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3305-3319Subventions
Organisme : British Heart Foundation
ID : CH/1999001/11735
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/20/3/34823
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE/18/2/34213
Pays : United Kingdom
Informations de copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.
Déclaration de conflit d'intérêts
Conflict of interest: A.M.S. serves as an adviser to Forcefield Therapeutics and CYTE—Global Network for Clinical Research. This manuscript was handled by Reviews Deputy Editor Dr Ali J. Marian. None of the other authors declare any conflict of interest.
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