ccx282-b and Liver-Neoplasms

The number of patients with non-alcoholic steatohepatitis (NASH) is increasing globally. Recently, specific chemokine receptors have garnered interest as therapeutic targets in NASH. This is the first report to examine the role of the C-C chemokine receptor 9 (CCR9)/C-C chemokine receptor ligand 25 (CCL25) axis, and to reveal its therapeutic potential in NASH.. Patients with biopsy-proven non-alcoholic liver disease (NAFLD) were recruited and their serum and hepatic chemokine expression was examined. Furthermore, wild-type (WT) and Ccr9. Serum CCL25, and hepatic CCR9 and CCL25 expression levels were increased in patients with NASH compared to healthy volunteers. Furthermore, Ccr9. These results highlight the role of the CCR9/CCL25 axis on macrophage recruitment and fibrosis formation in a murine NASH model, providing new insights into therapeutic strategies for NASH.. Herein, we show that a specific chemokine axis involving a receptor (CCR9) and its ligand (CCL25) contributes to the progression of non-alcoholic steatohepatitis and carcinogenesis in humans and mice. Furthermore, treatment with a CCR9 antagonist ameliorates the development of steatohepatitis and holds promise for the treatment of patients with non-alcoholic steatohepatitis.

Topics: Adult; Aged; Animals; Carcinoma, Hepatocellular; Case-Control Studies; Chemokines, CC; Diet, High-Fat; Disease Models, Animal; Disease Progression; Female; Hepatic Stellate Cells; Humans; Liver; Liver Neoplasms; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Middle Aged; Non-alcoholic Fatty Liver Disease; Receptors, CCR; Sulfonamides; Treatment Outcome