LGALS3 and cardiac hypertrophy: Recent studies suggest that the targets of galectin-3 in myocardial fibroblasts and extracellular matrix, together with activated myocardial macrophages, can induce fibroblast activation and proliferation, stimulate infiltration of macrophages and mast cells, increase myocardial interstitial deposition of molecules such as type I collagen around the heart and blood vessels, and cause myocardial hypertrophy and decreased myocardial compliance, which ultimately lead to heart failure (42).