ArticleEuropean heart journal2019
Activated platelets promote an osteogenic programme and the progression of calcific aortic valve stenosis.
Article in European heart journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 86 citations in OpenAlex.
- Aortic valve disease: Novel animal models for advancing our understanding of the underlying mechanisms.Animal models and experimental medicine · 2026Review
- Detrimental Effect of Plasma From Patients With Severe Aortic Stenosis on Valvular Endothelial Cells: Role of Proinflammatory Cytokines and Factor Xa.Journal of the American Heart Association · 2026Article
- Specific serotonin receptor antagonist reduces murine calcific atherosclerosis.Atherosclerosis · 2026Article
- New Insights Into the Diagnosis and Management of Aortic Stenosis.JACC. Asia · 2026Article
- Circulating serotonin is associated with calcific aortic valve stenosis: a two-phase metabolomics study.Frontiers in pharmacology · 2026Article
- Peripheral Serotonergic Activation in Severe Aortic Stenosis: A Biochemical Perspective.International journal of molecular sciences · 2025Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Plasma-Derived Extracellular Vesicle-Propagated microRNA From Aortic Stenosis Patients Render Pro-Calcifying Effects on Valve Interstitial Cells.JACC. Basic to translational science · 2025Article
- Platelet-Related Biomarkers and Efficacy of Antiplatelet Therapy in Patients with Aortic Stenosis and Coronary Artery Disease.International journal of molecular sciences · 2025Article
- Biomarkers of Calcification, Endothelial Injury, and Platelet-Endothelial Interaction in Patients with Aortic Valve Stenosis.International journal of molecular sciences · 2025Article
- Navigating the Landscape of Translational Medicine of Calcific Aortic Valve Disease: Bridging Bench to Bedside.JACC. Asia · 2025Review
- Calcific aortic stenosis: omics-based target discovery and therapy development.European heart journal · 2025Review
- Effects of LP533401 on vascular and bone calcification in hyperlipidemic mice.Biochemical and biophysical research communications · 2024Article
- Autotaxin inhibition attenuates the aortic valve calcification by suppressing inflammation-driven fibro-calcific remodeling of valvular interstitial cells.BMC medicine · 2024Article
- Evidence That Anemia Accelerates AS Progression Via Shear-Induced TGF-β1 Activation: Heyde's Syndrome Comes Full Circle.JACC. Basic to translational science · 2024Article
- Expression of miR-223 to predict outcomes after transcatheter aortic valve implantation.Cardiology journal · 2024Article
- Influence of Aortic Valve Stenosis and Wall Shear Stress on Platelets Function.Journal of clinical medicine · 2023Review
- Calcific aortic valve disease: mechanisms, prevention and treatment.Nature reviews. Cardiology · 2023Review
- Antiphospholipid antibodies in patients with calcific aortic valve stenosis.Rheumatology (Oxford, England) · 2023Article
- PTP1B Inhibition Improves Mitochondrial Dynamics to Alleviate Calcific Aortic Valve Disease Via Regulating OPA1 Homeostasis.JACC. Basic to translational science · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsCalcific aortic valve stenosis (CAVS) is characterized by a fibrocalcific process. Studies have shown an association between CAVS and the activation of platelets. It is believed that shear stress associated with CAVS promotes the activation of platelets. However, whether platelets actively participate to the mineralization of the aortic valve (AV) and the progression of CAVS is presently unknown. To identify the role of platelets into the pathobiology of CAVS. METHODS AND
resultsExplanted control non-mineralized and mineralized AVs were examined by scanning electron microscope (SEM) for the presence of activated platelets. In-depth functional assays were carried out with isolated human valve interstitial cells (VICs) and platelets as well as in LDLR-/- apoB100/100 IGFII (IGFII) mice. Scanning electron microscope and immunogold markings for glycoprotein IIb/IIIa (GPIIb/IIIa) revealed the presence of platelet aggregates with fibrin in endothelium-denuded areas of CAVS. In isolated VICs, collagen-activated platelets induced an osteogenic programme. Platelet-derived adenosine diphosphate induced the release of autotaxin (ATX) by VICs. The binding of ATX to GPIIb/IIIa of platelets generated lysophosphatidic acid (LysoPA) with pro-osteogenic properties. In IGFII mice with CAVS, platelet aggregates were found at the surface of AVs. Administration of activated platelets to IGFII mice accelerated the development of CAVS by 2.1-fold, whereas a treatment with Ki16425, an antagonist of LysoPA receptors, prevented platelet-induced mineralization of the AV and the progression of CAVS.
conclusionsThese findings suggest a novel role for platelets in the progression of CAVS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.