Plasma and Cardiac Galectin-3 in Patients With Heart Failure Reflects Both Inflammation and Fibrosis
نویسندگان
چکیده
Dysregulation of myocardial extracellular matrix remodeling and cardiac fibrosis is a key pathological feature of essentially any cardiovascular disease. Myocardial fibrosis contributes to the progression of heart failure and is linked to poor outcome in patients with cardiovascular disease. Consequently, predictors of myocardial fibrosis have been suggested as valuable markers of disease progression or measures of therapeutic success. Plasma or serum levels of galectin-3 (Gal-3), a member of the carbohydrate-binding protein family of lectins, are currently studied as a potential novel biomarker for cardiac fibrosis and adverse cardiac remodeling in heart failure. Experimental studies have implicated that Gal-3 is secreted by activated macrophages and mediates profibrotic processes in rodent models of heart failure. Gal-3 has been linked to enhanced myofibroblast proliferation, collagen production, macrophage infiltration, and cardiac hypertrophy, at least in part via stimulation of the transforming growth factor-β/SMAD3 signaling pathway.
منابع مشابه
Plasma and Cardiac Galectin-3 in Patients With Heart Failure Reflects Both Inflammation and Fibrosis: Implications for Its Use as a Biomarker.
BACKGROUND Galectin (Gal)-3 is a β-galactoside-binding lectin and currently intensely studied as a biomarker in heart failure. Gal-3 also exerts proinflammatory effects, at least in extracardiac tissues. Objective of this study was to characterize the relationship of plasma and myocardial Gal-3 levels with cardiac fibrosis and inflammation in patients with nonischemic dilated cardiomyopathy and...
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