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The Role of Galectin-3 in Heart Failure-The Diagnostic, Prognostic and Therapeutic Potential-Where Do We Stand?
Beata Zaborska1, Małgorzata Sikora-Frąc1, Krzysztof Smarż1
1Department of Cardiology, Centre of Postgraduate Medical Education, Grochowski Hospital, 04-073 Warsaw, Poland.
Insights
Galectin-3 (Gal-3) significantly contributes to heart failure (HF) by promoting cardiac fibrosis and remodeling. Research explores Gal-3
Area of Science:
- Cardiology and Molecular Biology
- Biomarkers in Cardiovascular Disease
Background:
- Heart failure (HF) is a growing clinical syndrome with high morbidity and mortality.
- Galectin-3 (Gal-3) is implicated in HF pathophysiology, particularly cardiac fibrosis, inflammation, and ventricular remodeling.
- Cardiac fibrosis is a key feature of HF and atrial fibrillation.
Purpose of the Study:
- To review the role of Gal-3 in the pathogenesis of HF.
- To explore the clinical diagnostic and prognostic significance of Gal-3 in HF.
- To discuss Gal-3's potential as a therapeutic target for HF.
Main Methods:
- Review of existing literature on Gal-3 structure and function in HF.
- Analysis of studies correlating Gal-3 serum concentration with echocardiographic and CMR biomarkers in HF.
- Discussion of Gal-3's utility in various HF settings (acute/chronic, preserved/reduced ejection fraction).
Main Results:
- Gal-3 plays a crucial role in molecular mechanisms driving HF development.
- Numerous studies link elevated Gal-3 serum levels to HF biomarkers.
- Gal-3 shows potential for diagnosis, prognosis, and risk stratification in HF.
Conclusions:
- Gal-3 is a significant factor in HF pathogenesis, particularly fibrosis and remodeling.
- Gal-3 serum concentration is associated with HF severity and biomarkers.
- Gal-3 represents a promising therapeutic target for managing heart failure.
Abstract:
Heart failure (HF) is a clinical syndrome with high morbidity and mortality, and its prevalence is rapidly increasing. Galectin-3 (Gal-3) is an important factor in the pathophysiology of HF, mainly due to its role in cardiac fibrosis, inflammation, and ventricular remodeling. Fibrosis is a hallmark of cardiac remodeling, HF, and atrial fibrillation development. This review aims to explore the involvement of Gal-3 in HF and its role in the pathogenesis and clinical diagnostic and prognostic significance. We report data on Gal-3 structure and molecular mechanisms of biological function crucial for HF development. Over the last decade, numerous studies have shown an association between echocardiographic and CMR biomarkers in HF and Gal-3 serum concentration. We discuss facts and concerns about Gal-3's utility in acute and chronic HF with preserved and reduced ejection fraction for diagnosis, prognosis, and risk stratification. Finally, we present attempts to use Gal-3 as a therapeutic target in HF.
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