THE STATUS OF GALECTIN-3 IN DIFFERENT PHENOTYPES OF CHRONIC HEART FAILURE

Chronic heart failure (CHF) is currently considered one of the most pressing medical and socioeconomic problems worldwide, characterized by high morbidity and mortality rates, frequent hospitalizations, and a significant reduction in patients' quality of life. Its different phenotypes—heart failure with preserved ejection fraction (HFpEF), heart failure with mildly reduced ejection fraction (HFmrEF), and heart failure with reduced ejection fraction (HFrEF)—differ in their clinical course, pathogenetic mechanisms, and structural and functional changes in the myocardium. One of the major mechanisms contributing to CHF progression is myocardial fibrosis, which is associated with excessive accumulation of extracellular matrix components, increased myocardial stiffness, and impaired cardiac function. Galectin-3 is an important biomarker involved in inflammatory and fibrotic processes, particularly macrophage activation, fibroblast proliferation, and collagen synthesis. Increased galectin-3 concentrations may reflect enhanced profibrotic activity and pathological myocardial remodeling. Therefore, determining serum galectin-3 levels in patients with different CHF phenotypes may provide valuable information about the intensity of fibrotic processes and their relationship with structural and functional myocardial changes. Studying this biomarker is important for improving the understanding of CHF pathogenesis and identifying additional approaches to assessing myocardial fibrosis and disease progression.