ArticlePloS one2017
FLT-1 gene polymorphisms and protein expression profile in rheumatoid arthritis.
Article in PloS one, 2017. 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.
- Beyond PAD Inhibition: Emerging Avenues and Natural Products for Targeting Citrullination in Immune Diseases.Biomedicines · 2026Review
- Decoy Receptors in Autoimmunity: Molecular Guardians and Pathogenic Players in Immune Dysregulation.Mediators of inflammation · 2026Review
- Angiogenesis in rheumatoid Arthritis: Pathological characterization, pathogenic mechanisms, and nano-targeted therapeutic strategies.Bioactive materials · 2025Review
- Article
- Gene polymorphisms and serum levels of sVEGFR-1 in patients with systemic lupus erythematosus.Scientific reports · 2020Article
- Serum Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-1 Levels in Patients With Fibromyalgia Syndrome.Archives of rheumatology · 2019Article
- KDR (VEGFR2) Genetic Variants and Serum Levels in Patients with Rheumatoid Arthritis.Biomolecules · 2019Article
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8 authors.
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Abstract
objectivesInflammation and angiogenesis are a significant element of pathogenesis in rheumatoid arthritis (RA). The FLT-1- triggering factor for production of proinflammatory cytokines-might contributes to inflammation in patients with RA. Association of the FLT-1 polymorphisms with different "angiogenic diseases" suggests that it may be a novel genetic risk factor also for RA. The aim of the study was to identify FLT-1 genetic variants and their possible association with sFLT-1 levels, susceptibility to and severity of RA.
methodsThe FLT-1 gene polymorphisms were genotyped for 471 RA patients and 684 healthy individuals. Correlation analysis was performed with clinical parameters, cardiovascular disease (CVD) and anti-citrullinated peptide/protein antibody (ACPA) presence. The sFLT-1 serum levels were evaluated.
resultsThe FLT-1 gene polymorphisms showed no significant differences in the proportion of cases and controls. Furthermore, the FLT-1 rs2296188 T/C polymorphism was associated with ACPA-positive RA. Overall, rs9943922 T/C and rs2296283 G/A are in almost completed linkage disequilibrium (LD) with D' = 0.97 and r2 = 0.83. The FLT-1 rs7324510 A allele has shown association with VAS score (p = 0.035), DAS-28 score (p = 0.013) and ExRA presence (p = 0.027). Moreover, other clinical parameters were also higher in RA patients with this allele. In addition, FLT-1 genetic variants conferred higher sFLT-1 levels in RA patients compared to controls.
conclusionFLT-1 rs7324510 C/A variant may be a new genetic risk factor for severity of RA. Examined factor highly predispose to more severe disease activity as well as higher sFLT-1 levels in RA.
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