LGALS3 and Myocardial fibrosis: In addition, Gal-3 is a matricellular glycan-binding protein involved in myocardial fibrosis and remodeling, and activation of Gal-3 leads to its multimerization and formation of Gal-3 lattices on the cell surface, which enhance fibrotic signaling by trapping the TGF-β receptor on the cell surface, and these signaling factors, along with mechanical stresses, promote the transition of quiescent fibroblasts to active, collagen-producing myofibroblasts, thereby inducing the onset of myocardial fibrosis (73, 139, 140).