ArticleGenes & diseases2018
Anti-endothelial cell antibody rich sera from rheumatic heart disease patients induces proinflammatory phenotype and methylation alteration in endothelial cells.
Article in Genes & diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Immune cells and rheumatic heart disease: A 2-sample and Bayesian weighted Mendelian randomization study.Medicine · 2026Article
- Valve biology and rheumatic heart disease pathogenesis.Nature cardiovascular research · 2026Review
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- Rheumatic heart disease burden and determinants in cardiac patients: A follow up care concern in Ethiopia.International journal of cardiology. Cardiovascular risk and prevention · 2025Article
- Application of Transthoracic Echocardiography for Cardiac Safety Evaluation in the Clinical Development Process of Vaccines Against Streptococcus pyogenes.Drugs in R&D · 2024Review
- The Role of Inflammation and Oxidative Stress in Rheumatic Heart Disease.International journal of molecular sciences · 2022Review
- The Immune and Inflammatory Basis of Acquired Pediatric Cardiac Disease.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatic heart disease (RHD) is a major cause of cardiovascular morbidity and mortality in developing nations like India. RHD commonly affects the mitral valve which is lined by a single layer of endothelial cells (ECs). The role of ECs in mitral valve damage during RHD is not well elucidated. In here, anti-endothelial cell antibody from RHD patients has been used to stimulate the ECs (HUVECs and HMVECs). ECs proinflammatory phenotype with increased expression of TNFα, IL-6, IL-8, IFNγ, IL-1β, ICAM1, VCAM1, E-selectin, laminin B, and vimentin was documented in both ECs. The promoter hypomethylation of various key inflammatory cytokines (TNFα, IL-6, and IL-8), integrin (ICAM1) associated with leukocyte transendothelial migration, and extracellular matrix genes (vimentin, and laminin) were also observed. Further, the
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