Loss of TRIM67 Attenuates the Progress of Obesity-Induced Non-Alcoholic Fatty Liver Disease.
NAFLD
TRIM67
inflammation
obesity
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 Jul 2022
05 Jul 2022
Historique:
received:
13
06
2022
revised:
01
07
2022
accepted:
02
07
2022
entrez:
9
7
2022
pubmed:
10
7
2022
medline:
14
7
2022
Statut:
epublish
Résumé
Obesity is considered as a major cause for the development and progress of non-alcoholic fatty liver disease (NAFLD), which is one of the most prevalent chronic liver diseases worldwide. However, molecular mechanisms that implicate in obesity-driven pathophysiology of NAFLD are not well defined. Here, we report a tripartite motif (TRIM) protein family member-TRIM67-that is hardly expressed in liver but is inducible on obese conditions. Enhanced expression of TRIM67 activates hepatic inflammation to disturb lipid metabolic homeostasis and promote the progress of NAFLD induced by obesity, while the deficiency in TRIM67 is protective against these pathophysiological processes. Finally, we show that the important transcription coactivator PGC-1α implicates in the response of hepatic TRIM67 to obesity.
Identifiants
pubmed: 35806477
pii: ijms23137475
doi: 10.3390/ijms23137475
pmc: PMC9267895
pii:
doi:
Substances chimiques
Cytoskeletal Proteins
0
TRIM67 protein, human
0
Tripartite Motif Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Natural Science Foundation of China
ID : 31871179
Organisme : Sichuan international science and technology innovation cooperation project
ID : 2020YFH0148
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