CCL2 and metabolic dysfunction-associated steatotic liver disease: When NAFLD progresses to NASH, the LSECs display a pro-inflammatory phenotype characterized by the surface overexpression of adhesion molecules such as ICAM-1, VCAM-1, and VAP-1 (AOC3) and the production of pro-inflammatory molecules, including TNF-α, IL-6, IL-1, and MCP1 (CCL2), as observed in experiments in mouse models of NASH [95,104].