[The involvement of galectin-3 in heart failure]

Hart failure (HF) accounts for numerous serious problems: medical, social and financial. HF affects 2-3% adult population and its frequency increases with age. Despite advances in laboratory diagnostics of HR the use of biochemical markers remains limited. Currently, only natriuretic peptides, especially type B natriuretic peptides (BNP) and N-terminal fragment of pro-BNP (NT-proBNP) have been fully approved biomarkers employed in diagnosing HF. The concentration of those peptides fluctuates and largely depends on age, gender, renal function, day/night rhythm and volemia which reflects hemodynamic state rather than hart abnormal structure. As the application of natriuretic peptides is limited in certain groups of patients, it is necessary to search for other more stable biomarkers. Recent investigations have suggested galectin-3 (gal-3) to be a new promising cardiological marker. Gal-3 belongs to a family of lectins that demonstrate binding specificity for β-galactoside which are produced by activated macrophages. Its operative path involves stimulation of cardiac fibroblasts and collagen production which can result in pathological remodeling of the myocardium structure. Numerous research found substantially increased gal-3 level in patients with chronic HF disregarding the etiology of disease. Moreover, some clinical studies have proved that increased gal-3 concentration is a factor of poor prognosis and predicative of death due to any reason in patients with HF. Contrary to natriuretic peptides, gal-3 is hemodynamically stable which is an additional asset of gal-3 as a marker of myocardial fibrosis.The article presents current state of research into gal-3 involvement in HF pathogenesis and possible use of gal-3 as a diagnostic marker of HF.