CCL2 and metabolic dysfunction-associated steatohepatitis: Furthermore, macrophage-derived FGF12 and Tim3 have been shown to differentially activate HSCs through distinct mechanisms via the Monocyte Chemoattractant Protein-1 (MCP-1)/CCR2 axis and TGF-β secretion, respectively, all of which contribute to MASH pathogenesis (110, 111).