Fig. 1.

Potential role of CD11c-positive macrophages and activated fibroblasts in the progression from hepatic steatosis to NASH and HCC

During the development of NASH, resident macrophages (Kupffer cells) aggregate around dying or dead hepatocytes to constitute hCLS, and these macrophages become CD11c-positive in response to hepatocyte death, with unique gene expression profiles. Metabolic stress such as saturated fatty acids induces FGF9 expression in activated fibroblasts, thereby increasing cell migration and viability of fibroblasts and hepatoma cells, and thus promoting tumor growth.