ArticleCommunications biology2026
The secretory protein, CLCF1, improves cholestatic liver disease by inhibiting hepatic bile acid synthesis and promoting bile acid excretion.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cholestatic liver disease (CLD) is characterized by disrupted bile acid (BA) homeostasis and excessive accumulation of toxic bile acids in the liver. While both genetic and acquired factors are known to contribute to its pathogenesis, the full spectrum of underlying pathological mechanisms remains incompletely understood, and treatment options are limited. Cardiotrophin-like cytokine factor 1 (CLCF1), a CNTFR ligand, plays a pivotal role in energy metabolic homeostasis, yet its role in cholestasis remains unclear. Here, we show that hepatic CLCF1 expression is markedly upregulated in cholestatic patients and mouse models (all mice used in this study were male). Hepatocyte-specific Cntfr deletion exacerbates DDC-induced cholestasis and fibrosis, whereas AAV-mediated hepatic Clcf1 overexpression attenuates cholestatic liver injury and fibrosis in both Abcb4 knockout (Mdr2
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