ArticleClinical and molecular hepatology2022
Galectin-3 inhibits cardiac contractility via a tumor necrosis factor alpha-dependent mechanism in cirrhotic rats.
Article in Clinical and molecular hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Heart failure with preserved ejection fraction beyond the heart: exploring the heart-liver-pancreas axis.ESC heart failure · 2026Review
- Cirrhotic cardiomyopathy: pathophysiology, assessment, and implications for liver transplantation.Therapeutic advances in gastroenterology · 2026Review
- Cirrhotic Cardiomyopathy: Bridging Hepatic and Cardiac Pathophysiology in the Modern Era.Journal of clinical medicine · 2025Review
- Apoptosis in Cardiac Conditions Including Cirrhotic Cardiomyopathy.International journal of molecular sciences · 2025Review
- Therapies for Cirrhotic Cardiomyopathy: Current Perspectives and Future Possibilities.International journal of molecular sciences · 2024Review
- Cardiomyopathy in cirrhosis: From pathophysiology to clinical care.JHEP reports : innovation in hepatology · 2024Review
- Chenodeoxycholic Acid Improves Embryo Implantation and Metabolic Health through Modulating Gut Microbiota-Host Metabolites Interaction during Early Pregnancy.Antioxidants (Basel, Switzerland) · 2023Article
- Temporal profile of cerebrospinal fluid galactin-3 and associated cytokine responses after severe traumatic brain injury in patients: a retrospective study.Future healthcare journal · 2023Article
- Role of Galectin in Cardiovascular Conditions including Cirrhotic Cardiomyopathy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Pathogenic Mechanisms Underlying Cirrhotic Cardiomyopathy.Frontiers in network physiology · 2022Review
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsGalectin-3 plays a key pathogenic role in cardiac hypertrophy and heart failure. The present study aimed to investigate the effects of galectin-3 on cardiomyopathy - related factors and cardiac contractility in a rat model of cirrhotic cardiomyopathy.
methodsRats were divided into two sets, one for a functional study, the other for cardiac contractile-related protein evaluation. There were four groups in each set: sham operated and sham plus N-acetyllactosamine (N-Lac, a galectin-3 inhibitor; 5 mg/kg); bile duct ligated (BDL) and BDL plus N-Lac. Four weeks after surgery, ventricular level of galectin-3, collagen I and III ratio, tumor necrosis factor alpha (TNFα), and brain natriuretic peptide (BNP) were measured either by Western blots or immunohistochemistry or enzyme-linked immunosorbent assay. Blood pressure was measured by polygraph recorder. Cardiomyocyte contractility was measured by inverted microscopy.
resultsGalectin-3 and collagen I/III ratio were significantly increased in cirrhotic hearts. TNFα and BNP were significantly increased in BDL serum and heart compared with sham controls. Galectin-3 inhibitor significantly decreased galectin-3, TNFα, and BNP in cirrhotic hearts but not in sham controls. N-Lac also significantly improved the blood pressure, and systolic and diastolic cardiomyocyte contractility in cirrhotic rats but had no effect on sham controls.
conclusionIncreased galectin-3 in the cirrhotic heart significantly inhibited contractility via TNFα. Inhibition of galectin-3 decreased the cardiac content of TNFα and BNP and reversed the decreased blood pressure and depressed contractility in the cirrhotic heart. Galectin-3 appears to play a pathogenic role in cirrhotic cardiomyopathy.
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