Both Gal-3 and α-SMA expression levels remain higher in the UUO model [28], continuously increasing macrophage recruitment, and probably justifying the clearly higher level of renal fibrosis observed in the UUO model by directly acting through TGF-β1-mediated myofibroblast activation and extracellular matrix production [46]. This evidence concerns the gene LGALS3 and renal fibrosis.