ArticleJournal of the American Heart Association2026
Detrimental Effect of Plasma From Patients With Severe Aortic Stenosis on Valvular Endothelial Cells: Role of Proinflammatory Cytokines and Factor Xa.
Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review
- Mechanistic insights into SGLT2 inhibition in Takotsubo syndrome.European heart journal. Cardiovascular pharmacotherapy · 2026Article
- Human Plasma in Calcific Aortic Valve Disease: Not Simply a Depot of Biomarkers.Journal of the American Heart Association · 2026Article
- Unmasking the Hidden Burden: Inflammation and Cardiovascular DiseaseJournal of the American Heart Association · 2026Article
- Impact of Anticoagulant Class on Long-Term Bioprosthesis Durability Following Transcatheter Aortic Valve Replacement.Structural heart : the journal of the Heart Team · 2026Article
- Assessing Potential Valve-Preserving Effects of SGLT2 Inhibitors in Degenerative Aortic Stenosis: A Propensity-Matched Study.Journal of clinical medicine · 2026Article
- Association of SGLT2 Inhibitors with Mortality and Bioprosthesis Valve Failure After TAVR: A Propensity-Matched Cohort Study.Journal of clinical medicine · 2025Article
- Subclinical Leaflet Thrombosis and Subclinical Aortic Valve Complex Thrombosis in TAVR.JACC. Advances · 2025Review
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15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of plasma and its components in the progression of aortic stenosis (AS) remains insufficiently investigated. This study aimed to assess whether plasma from patients with AS induces oxidative stress and contributes to valvular endothelial cells (VECs) dysfunction.
methodsHuman plasma samples were obtained from patients with severe AS (AS+, n=110), patients with cardiovascular risk factors without AS (n=30), and healthy individuals (n=15). Plasma levels of proinflammatory cytokines (IL [interleukin]-1β, IL-6, TNF [tumor necrosis factor]-α, and factor Xa [FXa]) were measured. Porcine aortic VECs were then incubated with plasma (10%, 24 hours). Oxidative stress levels were assessed using dihydroethidium staining, NO formation with 4-amino-5-methylamino-2',7'-difluororescein diacetate, mRNA expression by quantitative reverse transcription-polymerase chain reaction, and protein expression levels by Western blot analyses. Platelets and monocytes adhesion as well as thrombin generation were determined. Different pharmacological inhibitors were used to explore the underlying pathways.
resultsPlasma from patients with AS+ exhibited elevated levels of IL-1β, IL-6, TNF-α, and FXa activity. Incubation of VECs with AS+ plasma induced a pro-oxidant response mediated by proinflammatory cytokines, the angiotensin system-SGLT2 (sodium-glucose transport protein 2) pathway, and FXa. AS+ plasma also triggered VEC dysfunction, inflammation, monocytes and platelets adhesion, and thrombin generation. These detrimental effects were mitigated by empagliflozin, losartan, neutralizing antibodies targeting proinflammatory cytokines, and dabigatran and rivaroxaban.
conclusionsPatients with AS displayed subclinical systemic inflammation and increased FXa activity. These processes contributed to aortic VEC dysfunction, inflammation, monocytes and platelets adhesion, and thrombin generation upon exposure to AS+ plasma.
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