Notably, senescent hepatocytes accumulate with age and MASLD severity; they lose β-oxidation capacity and secrete senescence-associated secretory phenotype (SASP) cytokines rich in IL-6, IL-1β, and monocyte chemoattractant protein 1 (MCP-1), which trigger NOD-like receptor family pyrin domain containing 3 (NLRP3) systemically [62]. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatotic liver disease.