This study demonstrates that CCL2 is a key molecule for the development of metabolic and histological alterations in the liver of mice sensitive to the development of hyperlipidemia and hepatic steatosis, a finding with potential to identify new therapeutic targets in liver diseases.
Indeed, CD44 enhances the non-alcoholic fatty liver (NAFL) (hepatic steatosis) to NASH progression by regulating hepatic macrophage polarization (pro-inflammatory phenotype) and infiltration (macrophage motility and the MCP1/CCL2/CCR2 system).
These findings suggest that an increase in MCP-1 expression in adipose tissue contributes to the macrophage infiltration into this tissue, insulin resistance, and hepatic steatosis associated with obesity in mice.