Upregulated galectin-3 is not a critical disease mediator of cardiomyopathy induced by beta_2-adrenoceptor overexpression

摘要

Preclin-ical studies have demonstrated that anti-galectin-3 (Gal-3) interventions are effective in attenuating cardiac remodeling, fibrosis, and dysfunction. We determined, in a transgenic (TG) mouse model of fibrotic caidiomyopathy, whether Gal-3 expression was elevated and whether Gal-3 played a critical role in disease development. We studied mice with fibrotic cardiomyopathy attributable to cardiac overexpression of human P2-adrenoceptors (beta_2-TG). Cardiac expression levels of Gal-3 and fibrotic or inflammatory genes were determined.