Msln/Muc16 signaling in activated Portal Fibroblasts drives the development of cholestatic fibrosis and HCC in aged female Mdr2-/- mice - PubMed
3 hours ago
- #Portal Fibroblasts
- #Cholestatic Fibrosis
- #Hepatocellular Carcinoma
- Aged female Mdr2-/- mice show increased susceptibility to cholestatic fibrosis and HCC compared to males.
- Deletion of Msln or Muc16 reduces fibrosis, inflammation, and HCC in Mdr2-/- mice, unlike deletion of Thy-1.
- Msln- and Muc16-deficient activated portal fibroblasts exhibit a less fibrogenic and inflammatory phenotype.
- MMP3 from Msln-/- aPFs mediates shedding of hepatic HGFR, suppressing hepatocyte proliferation via HGF-c-Met signaling.
- Inhibition of MMP3 restores proliferation in human hepatocytes, linking aPF signaling to hepatocyte function regulation.