Key result
Serum galectin-3 levels across heart failure phenotypes may track myocardial fibrosis and structural remodeling.
Why the study?
Different chronic heart failure phenotypes vary in pathogenetic mechanisms and structural changes, and evaluating serum galectin-3 levels across HFpEF, HFmrEF, and HFrEF may help clarify the intensity of myocardial fibrosis and disease progression.
Evaluating serum galectin-3 levels across different chronic heart failure phenotypes (HFpEF, HFmrEF, HFrEF) may help characterize the intensity of myocardial fibrosis and its association with structural and functional cardiac remodeling.
Answers are grounded in this paper and cite their sources.
Galectin-3 may mark fibrosis across HF phenotypes; leaves open its role in risk stratification or phenotype-specific therapy.
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.
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A.G. et al. (2026) conducted a review in Chronic heart failure (HFpEF, HFmrEF, HFrEF). Serum galectin-3 was evaluated on Myocardial fibrosis and structural/functional myocardial changes. Serum galectin-3 levels across CHF phenotypes (HFpEF, HFmrEF, HFrEF) may reflect fibrotic intensity and myocardial remodeling, though no quantitative results were reported in the abstract.
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