ArticleThe American journal of pathology2016
Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
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Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.
- Biomarkers as predictors of recurrence of atrial fibrillation post ablation: an updated and expanded systematic review and meta-analysis.Clinical research in cardiology : official journal of the German Cardiac Society · 2022Pooled it
- Biomarkers Associated with Mortality in Aortic Stenosis: A Systematic Review and Meta-Analysis.Medical sciences (Basel, Switzerland) · 2021Pooled it
- Psychosocial stress exacerbates doxorubicin-induced cardiotoxicity in adult C57BL/6N mice.Research square · 2026Article
- From Natriuretic Peptides to microRNAs: Multi-Analyte Liquid Biopsy Horizons in Heart Failure.Biomolecules · 2025Review
- miR-210 overexpression increases pressure overload-induced cardiac fibrosis.Non-coding RNA research · 2025Article
- Article
- Circulating Biomarkers and Recurrence of Persistent Atrial Fibrillation After Electrical Cardioversion.Biomarker insights · 2025Article
- Emerging Role of Macrophage-Fibroblast Interactions in Cardiac Homeostasis and Remodeling.JACC. Basic to translational science · 2025Review
- Galectin-3 in acute myocardial infarction: from molecular mechanisms to clinical translation.Frontiers in molecular biosciences · 2025Review
- Association of suPAR, ST2, and galectin-3 with eGFR decline and mortality in patients with advanced heart failure with reduced ejection fraction.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2024Article
- Galectin-3 Predicts Long-Term Risk of Cerebral Disability and Mortality in Out-of-Hospital Cardiac Arrest Survivors.Journal of personalized medicine · 2024Article
- Proteomics couples electrical remodelling to inflammation in a murine model of heart failure with sinus node dysfunction.Cardiovascular research · 2024Article
- Conditioned Medium from Human Amniotic Membrane-Derived Mesenchymal Stem Cells Modulates Inflammatory and Myofibrotic Factors in Vivo.The journal of Tehran Heart Center · 2024Article
- Article
- Correlations of sST2 and Gal-3 with Cardiothoracic Ratio in Patients with Chronic Kidney Disease.Biomedicines · 2024Article
- Galectin-3 is involved in inflammation and fibrosis in arteriogenic erectile dysfunction via the TLR4/MyD88/NF-κB pathway.Cell death discovery · 2024Article
- Review
- Role of Galectin in Cardiovascular Conditions including Cirrhotic Cardiomyopathy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Plasma Galectin-3 and H-FABP correlate with poor physical performance in patients with congestive heart failure.Experimental biology and medicine (Maywood, N.J.) · 2023Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
The β-galactoside-binding animal lectin galectin-3 is predominantly expressed by activated macrophages and is a promising biomarker for patients with heart failure. Galectin-3 regulates inflammatory and fibrotic responses; however, its role in cardiac remodeling remains unclear. We hypothesized that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy and fibrosis. In normal mouse myocardium, galectin-3 was constitutively expressed in macrophages and was localized in atrial but not ventricular cardiomyocytes. In a mouse model of transverse aortic constriction, galectin-3 expression was markedly up-regulated in the pressure-overloaded myocardium. Early up-regulation of galectin-3 was localized in subpopulations of macrophages and myofibroblasts; however, after 7 to 28 days of transverse aortic constriction, a subset of cardiomyocytes in fibrotic areas contained large amounts of galectin-3. In vitro, cytokine stimulation suppressed galectin-3 synthesis by macrophages and cardiac fibroblasts. Correlation studies revealed that cardiomyocyte- but not macrophage-specific galectin-3 localization was associated with adverse remodeling and dysfunction. Galectin-3 knockout mice exhibited accelerated cardiac hypertrophy after 7 days of pressure overload, whereas female galectin-3 knockouts had delayed dilation after 28 days of transverse aortic constriction. However, galectin-3 loss did not affect survival, systolic and diastolic dysfunction, cardiac fibrosis, and cardiomyocyte hypertrophy in the pressure-overloaded heart. Despite its potential role as a prognostic biomarker, galectin-3 is not a critical modulator of cardiac fibrosis but may delay the hypertrophic response.
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