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Targeting the liver clock improves fibrosis by restoring TGF-β signaling.

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Crouchet, Emilie | Dachraoui, Mayssa | Jühling, Frank | Roehlen, Natascha | Oudot, Marine | Durand, Sarah C. | Ponsolles, Clara | Gadenne, Cloé | Meiss-Heydmann, Laura | Moehlin, Julien | Martin, Romain | Brignon, Nicolas | del Zompo, Fabio | Teraoka, Yuji | Aikata, Hiroshi | Abe-Chayama, Hiromi | Chayama, Kazuaki | Saviano, Antonio | Heide, Danijela | Onea, Mihaela | Geyer, Lucas | Wolf, Thibaut | Felli, Emanuele | Pessaux, Patrick | Heikenwälder, Mathias | Chambon, Pierre | Schuster, Catherine | Lupberger, Joachim | Mukherji, Atish | Baumert, Thomas F.

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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.

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