The Role of Galectin-3 and ST2 in Cardiology: A Short Review

Abstract

Galectin-3 is a lectin that binds beta-galactosides. It is involved in cardiac remodeling and fibrosis through the activation of macrophages and fibroblasts. ST2 is secreted by myocardial cells due to cardiac overload. These two biomarkers have been traditionally studied in the field of heart failure to guide medical therapy and detect the progression of the disease. Nevertheless, there are novel evidences that connect galectin-3 and ST2 with coronary heart disease and, specifically, with atrial fibrillation. The aim of this article is to concisely review the diagnostic and prognostic role of galectin-3 and ST2 in different cardiac diseases.

Exploring the Causal Effects of Circulating ST2 and Galectin-3 on Heart Failure Risk: A Mendelian Randomization Study

“…Considering to the aspect of HF risk in general population, our findings are not contradictory with previous studies. To some extent, circulating ST2 and galectin-3 are not cardiac-specific biomarkers ( 9 ). Concentration variation of these two mediators in serum is not parallel with that in myocardium.…”

“…As predictive biomarkers for prognosis of HF patients, both soluble ST2 and galectin-3 are extensively involved in inflammatory mechanisms resulting in myocardial fibrosis and adverse cardiac remodeling ( 8 ). However, the causal effects of these two mediators on the risk of HF are still not fully elucidated ( 9 ).…”

The Diagnostic and Therapeutic Potential of Galectin-3 in Cardiovascular Diseases

“…High GDF-15 concentrations were noted in hypertrophic and dilated cardiomyopathies, after volume overload, ischaemia and heart failure [ 86 ]. The ST2 receptor has two isoforms: membrane-bound receptor type 2 (ST2L) and soluble form (sST2), present in serum and most frequently used in diagnostic procedures [ 70 , 87 ]. The form sST2 is a “bait” for IL-33 and thus it counteracts its interaction with the membrane-bound ST2L, blocking the paracrine fibroblast-cardiomyocyte communication system and reducing the cardioprotective effect of IL-33 [ 87 ].…”

Role of New Potential Biomarkers in the Risk of Thromboembolism in Atrial Fibrillation

“…Galectin-3, a lectin that binds β-galactosides, is involved in cardiac remodeling and fibrosis through its effect of activating macrophages and fibroblasts. Various studies have documented that increased levels of circulating galectin-3 are associated with AF-related IS and LAA thrombus formation [48,49].…”