Genetic disruption of galectin-3 prevents adverse cardiac remodeling

 We measured cardiac function with echo (fractional shortening, FS%). Prior to sacrifice, invasive hemodynamics were recorded. Ventricular collagen deposition was quantified as fibrosis score (%) by histological analysis, and we measured markers of collagen metabolism in plasma by ELISA (procollagen type I/III Nterminal propeptides, PINP and PIIINP, respectively). Galectin-3 is a carbohydrate binding protein. Elevated levels of galectin-3 are associated with poor prognosis in human heart failure. In preclinical models, Galectin-3 was found to be a mediator of liver and kidney fibrosis. Additionally it has been shown that exposing the myocardium to Galectin-3 induces cardiac fibrogenesis and compromises function.