Hepatocyte-specific ANGPTL8 knockout or soluble PirB ectodomain treatment reduced monocyte-derived macrophage infiltration, lipid accumulation, and fibrosis progression in mouse models of NASH.
The PirB/LILRB2-ANGPTL8 signaling axis mediates macrophage recruitment and inflammatory activation in NASH, presenting a potential therapeutic target for NASH management.
bone marrow (BM) chimeras abrogate ANGPTL8-induced MDM migration to the liver. And yet, PirB ectodomain protein could ameliorate NASH by sequestering ANGPTL8. Furthermore, LILRB2-ANGPTL8 binding-promoted MDM migration and inflammatory activation are also observed in human peripheral blood monocytes. Taken together, our findings reveal the role of PirB/LILRB2 in NASH pathogenesis and identify PirB/LILRB2-ANGPTL8 signaling as a potential target for the management or treatment of NASH.
Li et al. (Sat,) conducted a other in Nonalcoholic steatohepatitis (NASH). Hepatocyte-specific ANGPTL8 knockout and soluble PirB ectodomain (sPirB) vs. Wild-type/vehicle controls was evaluated. Hepatocyte-specific ANGPTL8 knockout or soluble PirB ectodomain treatment reduced monocyte-derived macrophage infiltration, lipid accumulation, and fibrosis progression in mouse models of NASH.
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