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.
Sakane et al. (Wed,) studied this question.