A role for Galectin-3 in the development of early molecular alterations in short-term aortic stenosis

Aortic stenosis (AS) is characterized by pressure overload and causes left ventricular (LV) fibrosis and inflammation, two mechanisms which finally lead to cardiac dysfunction. Galectin-3 (Gal-3), a β-galactoside-binding lectin, promotes cardiac remodeling. We herein investigated the role of Gal-3 in LV remodeling in patients with AS and the effects of Gal-3 blockade in rats subjected to short-term (6-week) supravalvular aortic banding (AS group). Myocardial biopsies were obtained from 25 patients with severe AS referred for aortic valve replacement and from necropsies of 11 cardiovascular disease-free control subjects. Gal-3 was upregulated in myocardial biopsies from AS patients as compared to controls. Gal-3 directly correlated with parameters assessing myocardial fibrosis and inflammation in AS patients. Normotensive AS animals presented decreased LV diastolic diameter as compared to controls. At histological level, AS rats exhibited slight increase in LV cross sectional area and LV wall thickness and augmented cardiomyocyte width and cross sectional area. AS animals presented enhanced cardiac Gal-3 expression that paralleled higher myocardial fibrosis and inflammation. Cardiac Gal-3 was associated with fibrosis and inflammatory markers. Gal-3 pharmacological inhibition prevented the increase in cardiac Gal-3 and normalized histological and molecular alterations in AS rats.In short-term AS, the increase in myocardial Gal-3 expression was associated with car...
Source: Clinical Science - Category: Biomedical Science Authors: Tags: PublishAheadOfPrint Source Type: research