These findings demonstrate that aPFs mediate the cross-talk between cholangiocytes and hepatocytes, regulate hepatocyte functions, and that Msln-Muc16 signaling in aPFs is pathogenic for cholestatic fibrosis and HCC. Msln and Muc16 may become novel targets for anti-fibrotic therapy and HCC patients with sclerosis cholangitis.
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Sadatsugu Sakane
Takahiro Nishio
Hiroaki Fuji
Cellular and Molecular Gastroenterology and Hepatology
University of California, San Diego
Kyoto University
Discovery Institute
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Sakane et al. (Wed,) studied this question.
www.synapsesocial.com/papers/69df2a4be4eeef8a2a6af76b — DOI: https://doi.org/10.1016/j.jcmgh.2026.101785