LGALS3 and metabolic dysfunction-associated steatohepatitis: Consistently, galectin-3 secretion by macrophages has been implicated in the promotion of renal and vascular fibrosis,40,41 whereas genetic deletion or inhibition of galectin-3 attenuates HSC activation and hepatic collagen deposition in CCl4− or tioacetamide-treated mice19,42 and ameliorated inflammation and fibrosis in experimental NASH.43