Targeting the liver clock improves fibrosis by restoring TGF-β signaling.
Fiche publication
Date publication
août 2024
Journal
Journal of hepatology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAUMERT Thomas, Pr CHAMBON Pierre, Dr LUPBERGER Joachim, Pr PESSAUX Patrick, Dr MUKHERJI Atish, Dr CROUCHET Emilie
Tous les auteurs :
Crouchet E, Dachraoui M, Jühling F, Roehlen N, Oudot MA, Durand SC, Ponsolles C, Gadenne C, Meiss-Heydmann L, Moehlin J, Martin R, Brignon N, Del Zompo F, Teraoka Y, Aikata H, Abe-Chayama H, Chayama K, Saviano A, Heide D, Onea M, Geyer L, Wolf T, Felli E, Pessaux P, Heikenwälder M, Chambon P, Schuster C, Lupberger J, Mukherji A, Baumert TF
Lien Pubmed
Résumé
Liver fibrosis is the major driver for hepatocellular carcinoma and liver disease related death. Approved anti-fibrotic therapies are absent and compounds in development have limited efficacy. Increased TGF-β signaling drives collagen deposition by hepatic stellate cells (HSC)/myofibroblasts. Here, we aimed to dissect the role of the circadian clock (CC) in controlling TGF-β signaling and liver fibrosis.
Mots clés
Liver disease, MASLD, circadian clock, drug discovery, hepatic stellate cells, transcriptional regulation
Référence
J Hepatol. 2024 08 20;: