EphB2 deficiency in hepatic stellate cells mitigated MASH fibrosis in mice.

Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as the leading cause for liver transplantation worldwide. MASH is chatacterized by hepatic lipid accumulation, inlammation and fibrosis which is associaed with worst outcome in patients sufferreing from this pathology. Using the murine choline deficient amino acid defined high fat diet (CDAA-HFD) model of MASH we showed that Ephb2-specific deletion in HSCs using the tamoxifen inducible PdgfCre-eRT2 promoer driver is sufficient to mitigate MASH fibrosis in mice. Overall design: After tamoxifen administration (IP) to Ephb2flox/flox (Cre-) and Ephb2flox/flox-PdgfrbCreERT2 (cre+) eight to ten weeks old male mice for 5 consecutive days , they were then fed a Choline deficient L-Amino Acid defined (CDAA) high-fat diet (RESEARCH DIETS A16092003i 45%Kcal fat; 0.1% methionine; 1% Cholesterol; No added Choline) for 8 weeks.