Stimulates Short-Chain Dehydrogenase/Reductase Proteins to Alleviate Heart Failure Independent of Mitochondrial Protein Deacetylation.
NAD+
heart failure
mitochondria
nicotinamide riboside
short-chain dehydrogenase
sirtuin
Journal
Circulation
ISSN: 1524-4539
Titre abrégé: Circulation
Pays: United States
ID NLM: 0147763
Informations de publication
Date de publication:
15 Nov 2023
15 Nov 2023
Historique:
medline:
15
11
2023
pubmed:
15
11
2023
entrez:
15
11
2023
Statut:
aheadofprint
Résumé
Strategies to increase cellular NAD We induced cardiac dysfunction by pressure overload in SIRT3-deficient (knockout) mice and compared their response with nicotinamide riboside chloride treatment with wild-type mice. To model a therapeutic approach, we initiated the treatment in mice with established cardiac dysfunction and found nicotinamide riboside chloride improved mitochondrial function and blunted heart failure progression. Similar benefits were observed in wild-type and knockout mice. Boosting NAD These findings identify SDR proteins as important regulators of mitochondrial function and molecular targets of NAD
Sections du résumé
BACKGROUND
UNASSIGNED
Strategies to increase cellular NAD
METHODS
UNASSIGNED
We induced cardiac dysfunction by pressure overload in SIRT3-deficient (knockout) mice and compared their response with nicotinamide riboside chloride treatment with wild-type mice. To model a therapeutic approach, we initiated the treatment in mice with established cardiac dysfunction and found nicotinamide riboside chloride improved mitochondrial function and blunted heart failure progression. Similar benefits were observed in wild-type and knockout mice. Boosting NAD
CONCLUSIONS
UNASSIGNED
These findings identify SDR proteins as important regulators of mitochondrial function and molecular targets of NAD
Identifiants
pubmed: 37965787
doi: 10.1161/CIRCULATIONAHA.123.066039
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM