Remodeling of lipid landscape in high fat fed very-long chain acyl-CoA dehydrogenase null mice favors pro-arrhythmic polyunsaturated fatty acids and their downstream metabolites.
Calcium homeostasis
Endoplasmic reticulum stress
Lipidomic
Prostane
VLCAD deficiency
Journal
Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730
Informations de publication
Date de publication:
12 2023
12 2023
Historique:
received:
06
02
2023
revised:
20
07
2023
accepted:
04
08
2023
medline:
4
9
2023
pubmed:
10
8
2023
entrez:
9
8
2023
Statut:
ppublish
Résumé
Very-long chain acyl-CoA dehydrogenase (VLCAD) catalyzes the initial step of mitochondrial long chain (LC) fatty acid β-oxidation (FAO). Inherited VLCAD deficiency (VLCADD) predisposes to neonatal arrhythmias whose pathophysiology is still not understood. We hypothesized that VLCADD results in global disruption of cardiac complex lipid homeostasis, which may set conditions predisposing to arrhythmia. To test this, we assessed the cardiac lipidome and related molecular markers in seven-month-old VLCAD
Identifiants
pubmed: 37558007
pii: S0925-4439(23)00209-0
doi: 10.1016/j.bbadis.2023.166843
pii:
doi:
Substances chimiques
Acyl-CoA Dehydrogenase, Long-Chain
EC 1.3.8.8
Calcium
SY7Q814VUP
Fatty Acids
0
Fatty Acids, Unsaturated
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
166843Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors have no conflict of interest to declare.