Increased cardiac PFK-2 protects against high-fat diet-induced cardiomyopathy and mediates beneficial systemic metabolic effects.
Metabolomics
Molecular biology
Physiology
Proteomics
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
21 Jul 2023
21 Jul 2023
Historique:
received:
02
11
2022
revised:
27
04
2023
accepted:
10
06
2023
medline:
3
8
2023
pubmed:
3
8
2023
entrez:
3
8
2023
Statut:
epublish
Résumé
A healthy heart adapts to changes in nutrient availability and energy demands. In metabolic diseases like type 2 diabetes (T2D), increased reliance on fatty acids for energy production contributes to mitochondrial dysfunction and cardiomyopathy. A principal regulator of cardiac metabolism is 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2), which is a central driver of glycolysis. We hypothesized that increasing PFK-2 activity could mitigate cardiac dysfunction induced by high-fat diet (HFD). Wild type (WT) and cardiac-specific transgenic mice expressing PFK-2 (Glyco
Identifiants
pubmed: 37534142
doi: 10.1016/j.isci.2023.107131
pii: S2589-0042(23)01208-7
pmc: PMC10391959
doi:
Types de publication
Journal Article
Langues
eng
Pagination
107131Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM103447
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG050911
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL160955
Pays : United States
Organisme : NIGMS NIH HHS
ID : R24 GM137786
Pays : United States
Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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