Knock-Out of IKKepsilon Ameliorates Atherosclerosis and Fatty Liver Disease by Alterations of Lipid Metabolism in the PCSK9 Model in Mice.
Animals
Atherosclerosis
/ metabolism
Lipid Metabolism
Mice
Mice, Knockout
Proprotein Convertase 9
/ metabolism
I-kappa B Kinase
/ metabolism
Fatty Liver
/ metabolism
Disease Models, Animal
Diet, High-Fat
/ adverse effects
Liver
/ metabolism
Male
Plaque, Atherosclerotic
/ metabolism
Mice, Inbred C57BL
FASN
IKKε
PCSK9
SCD1
atherosclerosis
fatty liver disease
lipid
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:
05 Oct 2024
05 Oct 2024
Historique:
received:
17
09
2024
revised:
30
09
2024
accepted:
02
10
2024
medline:
16
10
2024
pubmed:
16
10
2024
entrez:
16
10
2024
Statut:
epublish
Résumé
The inhibitor-kappaB kinase epsilon (IKKε) represents a non-canonical IκB kinase that modulates NF-κB activity and interferon I responses. Inhibition of this pathway has been linked with atherosclerosis and metabolic dysfunction-associated steatotic liver disease (MASLD), yet the results are contradictory. In this study, we employed a combined model of hepatic PCSK9
Identifiants
pubmed: 39409049
pii: ijms251910721
doi: 10.3390/ijms251910721
pii:
doi:
Substances chimiques
Proprotein Convertase 9
EC 3.4.21.-
I-kappa B Kinase
EC 2.7.11.10
Pcsk9 protein, mouse
EC 3.4.21.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : GRK2336 and 445757098
Organisme : Hessian Ministry for Science and the Arts
ID : Theranova
Organisme : Fraunhofer Society
ID : Theranova