ArticleCirculation2020
Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis.
Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Genomic and transcriptomic analyses of aortic stenosis enhance therapeutic target discovery and disease prediction.Nature genetics · 2026Pooled it
- Aortic Stenosis Hyalectan Remodeling Revealed by Proteomics and Glycoproteomics.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- ChemR23 prevents phenotypic switching of vascular smooth muscle cells into macrophage-like foam cells in atherosclerosis.Cardiovascular research · 2026Article
- Considerations in the Use of Mouse Models of Vascular and Valvular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- The Emerging Roles of Resolvins: Potential Diagnostic Biomarkers for Cardiovascular Diseases.Current cardiology reviews · 2026Review
- Mechanisms of vascular calcification: cellular phenotype switching drives matrix remodeling and mineralized microenvironment formation.Frontiers in cardiovascular medicine · 2026Review
- Article
- Associations between per- and polyfluoroalkyl chemicals and abdominal aortic calcification in middle-aged and older adults.Journal of advanced research · 2025Article
- Calcific aortic stenosis: omics-based target discovery and therapy development.European heart journal · 2025Review
- Global burden of ischemic heart disease due to omega-3 deficiency: 204-country analysis, 1990-2021.Frontiers in nutrition · 2025Article
- Diabetes and calcific aortic valve disease: implications of glucose-lowering medication as potential therapy.Frontiers in pharmacology · 2025Review
- Type 2 Diabetes, Circulating Metabolites, and Calcific Aortic Valve Stenosis: A Mendelian Randomization Study.Metabolites · 2024Article
- TRPM4 mRNA stabilization by METTL3-mediated m6A modification promotes calcific aortic valve inflammation.Heliyon · 2024Article
- Is Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer.Metabolites · 2024Review
- Enhancing aortic valve drug delivery with PAR2-targeting magnetic nano-cargoes for calcification alleviation.Nature communications · 2024Article
- Post-stroke cognitive impairment: exploring molecular mechanisms and omics biomarkers for early identification and intervention.Frontiers in molecular neuroscience · 2024Review
- Structural basis of G protein-Coupled receptor CMKLR1 activation and signaling induced by a chemerin-derived agonist.PLoS biology · 2023Article
- Tomo-seq identifies NINJ1 as a potential target for anti-inflammatory strategy in thoracic aortic dissection.BMC medicine · 2023Article
- Calcific aortic valve disease: mechanisms, prevention and treatment.Nature reviews. Cardiology · 2023Review
- Differential expression profiles and functional analysis of long non-coding RNAs in calcific aortic valve disease.BMC cardiovascular disorders · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAortic valve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing of the aortic valve as a consequence of thickening and calcification of the aortic valve leaflets. The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular prevention have recently been demonstrated in a large randomized, controlled trial. In addition, n-3 PUFAs serve as the substrate for the synthesis of specialized proresolving mediators, which are known by their potent beneficial anti-inflammatory, proresolving, and tissue-modifying properties in cardiovascular disease. However, the effects of n-3 PUFA and specialized proresolving mediators on AVS have not yet been determined. The aim of this study was to identify the role of n-3 PUFA-derived specialized proresolving mediators in relation to the development of AVS.
methodsLipidomic and transcriptomic analyses were performed in human tricuspid aortic valves. Apoe
resultsWe found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified regions compared with calcified regions. Liquid chromatography tandem mass spectrometry-based lipid mediator lipidomics identified that the n-3 PUFA-derived specialized proresolving mediator resolvin E1 was dysregulated in calcified regions and acted as a calcification inhibitor. Apoe
conclusionsn-3 PUFA-derived resolvin E1 and its receptor ChemR23 emerge as a key axis in the inhibition of AVS progression and may represent a novel potential therapeutic opportunity to be evaluated in patients with AVS.
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