Hepatocyte Nuclear Factor 1α Proinflammatory Effect Linked to the Overexpression of Liver Nuclear Factor-κB in Experimental Model of Chronic Kidney Disease.
Animals
Cell Line, Tumor
Hepatocyte Nuclear Factor 1-alpha
Humans
Intercellular Adhesion Molecule-1
/ metabolism
Interleukin-6
/ genetics
Liver
/ metabolism
Models, Theoretical
NF-kappa B
/ genetics
RNA, Messenger
/ metabolism
Rats
Renal Insufficiency, Chronic
/ genetics
Transcription Factor RelA
/ genetics
Vascular Cell Adhesion Molecule-1
/ genetics
chronic kidney disease
clofibrate
hepatocyte nuclear factor 1α
intercellular cell adhesion molecule 1
interleukin-6
monocyte chemoattractant protein 1
nuclear factor–κB
vascular cell adhesion molecule 1
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:
10 Aug 2022
10 Aug 2022
Historique:
received:
11
07
2022
revised:
01
08
2022
accepted:
06
08
2022
entrez:
26
8
2022
pubmed:
27
8
2022
medline:
30
8
2022
Statut:
epublish
Résumé
Chronic kidney disease (CKD) is associated with low-grade inflammation that activates nuclear factor-κB (NF-κB), which upregulates the expression of numerous NF-κB responsive genes, including the genes encoding IL-6, ICAM-1, VCAM-1, and MCP-1. Herein, we found the coordinated overexpression of genes encoding RelA/p65 (a subunit of NF-κB) and HNF1α in the livers of chronic renal failure (CRF) rats-an experimental model of CKD. The coordinated overexpression of
Identifiants
pubmed: 36012158
pii: ijms23168883
doi: 10.3390/ijms23168883
pmc: PMC9408856
pii:
doi:
Substances chimiques
Hepatocyte Nuclear Factor 1-alpha
0
Interleukin-6
0
NF-kappa B
0
RNA, Messenger
0
Transcription Factor RelA
0
Vascular Cell Adhesion Molecule-1
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Références
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