By employing various genetically modified mice and experimental models of liver injury, the research team discovered upregulation of FGF18 in fibrotic livers. They observed that FGF18 promoted the proliferation of hepatic stellate cells in vitro and induced liver fibrosis in vivo. Furthermore, the team identified a correlation between the expressions of FGF18 and profibrotic genes in human biopsy samples. These findings strongly indicate that FGF18 plays a pivotal role in the progression of liver fibrosis.
The findings propose a potential therapeutic target for controlling liver fibrosis in chronic hepatitis by focusing on inhibiting or modulating FGF18. This discovery could pave the way for novel approaches to treating liver fibrosis, offering hope for patients with chronic hepatitis.
The results of the research were published in the scientific journal Nature Communications on October 9, 2023.