Over the last years a number of new biomarkers reflecting different aspects of heart failure (HF) pathophysiology have been evaluated in order to improve diagnosis and to better define prognosis of patients. Among these, Galectin 3 (Gal-3) seems particularly promising. It is a soluble beta galactoside-binding lectin produced by activated macrophages which binds and activates the fibroblasts thus leading to the deposition of collagen into the extracellular matrix and to a progressive cardiac fibrosis. Gal-3 plays also an important regulatory role in inflammatory status. Experimental studies have demonstrated that it is involved in cardiac remodeling and that it is one of the main determinants of development and progression of HF. In humans, Gal-3 plasma levels are associated with the onset of HF in apparently healthy patients and have been found being predictors of a worse prognosis in acute (AHF) as well as in chronic heart failure (CHF). Furthermore, Gal-3 serum levels are strongly correlated with renal dysfunction thus suggesting a possible role in better characterizing cardiorenal syndrome. The aim of this review was to revise the available experimental and clinical data concerning the role of Gal-3 as prognostic marker in HF.

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