ArticleInternational journal of molecular sciences2017
Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Preprocedural circulating galectin-3 and the risk of mortality after transcatheter aortic valve replacement: a systematic review and meta-analysis.Bioscience reports · 2020Pooled it
- Diastolic dysfunction is linked to the initiation and progression of aortic stenosis: a hypothesis.European heart journal · 2026Review
- Fibroblasts' secretome from calcified and non-calcified dermis in Pseudoxanthoma elasticum differently contributes to elastin calcification.Communications biology · 2024Article
- Mediating effect of vascular calcification in galectin-3-related mortality in hemodialysis patients.Scientific reports · 2024Article
- Serum and Vascular Stiffness Biomarkers Associated with the Severity of Degenerative Aortic Valve Stenosis and Cardiovascular Outcomes.Journal of cardiovascular development and disease · 2022Article
- Severe Aortic Valve Stenosis and Pulmonary Hypertension: A Systematic Review of Non-Invasive Ways of Risk Stratification, Especially in Patients Undergoing Transcatheter Aortic Valve Replacement.Journal of personalized medicine · 2022Review
- Galectin-3 promotes calcification of human aortic valve interstitial cells via the NF-kappa B signaling pathway.Cardiovascular diagnosis and therapy · 2022Article
- The Complex Biological Effects of Pectin: Galectin-3 Targeting as Potential Human Health Improvement?Biomolecules · 2022Review
- Role of Glycosylation in Vascular Calcification.International journal of molecular sciences · 2021Review
- Soluble St2 Induces Cardiac Fibroblast Activation and Collagen Synthesis via Neuropilin-1.Cells · 2020Article
- Soluble ST2, Galectin-3 and clinical prognosis of patients with hypertrophic cardiomyopathy undergoing ventricular septal myectomy: a correlation analysis.Cardiovascular diagnosis and therapy · 2020Article
- Pleiotropic Effects of Modified Citrus Pectin.Nutrients · 2019Review
- Letter to the Editor: Not all modified citrus pectins are the same: size does matter.American journal of physiology. Heart and circulatory physiology · 2019Article
- Echocardiographic diastolic function evolution in patients with an anterior Q-wave myocardial infarction: insights from the REVE-2 study.ESC heart failure · 2019Observational
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-3 (Gal-3) is involved in cardiovascular fibrosis and aortic valve (AV) calcification. We hypothesized that Gal-3 pharmacological inhibition with modified citrus pectin (MCP) could reduce aortic and AV remodeling in normotensive rats with pressure overload (PO). Six weeks after aortic constriction, vascular Gal-3 expression was up-regulated in male Wistar rats. Gal-3 overexpression was accompanied by an increase in the aortic media layer thickness, enhanced total collagen, and augmented expression of fibrotic mediators. Further, vascular inflammatory markers as well as inflammatory cells content were greater in aorta from PO rats. MCP treatment (100 mg/kg/day) prevented the increase in Gal-3, media thickness, fibrosis, and inflammation in the aorta of PO rats. Gal-3 levels were higher in AVs from PO rats. This paralleled enhanced AV fibrosis, inflammation, as well as greater expression of calcification markers. MCP treatment prevented the increase in Gal-3 as well as fibrosis, inflammation, and calcification in AVs. Overall, Gal-3 is overexpressed in aorta and AVs from PO rats. Gal-3 pharmacological inhibition blocks aortic and AV remodeling in experimental PO. Gal-3 could be a new therapeutic approach to delay the progression and the development of aortic remodeling and AV calcification in PO.
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Registered trials
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