ArticlePloS one2017
The rs7044343 Polymorphism of the Interleukin 33 Gene Is Associated with Decreased Risk of Developing Premature Coronary Artery Disease and Central Obesity, and Could Be Involved in Regulating the Production of IL-33.
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 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- IL-33/ST2 immunobiology in coronary artery disease: A systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2022Pooled it
- IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Interleukin (IL)-33 immunobiology in asthma and airway inflammatory diseases.The Journal of asthma : official journal of the Association for the Care of Asthma · 2022Article
- Innate-Immunity Genes in Obesity.Journal of personalized medicine · 2021Review
- Efficacy and safety of coronary stent intervention for coronary heart disease and its impact on short-term and long-term prognosis.American journal of translational research · 2021Article
- Article
- Interleukin-33 gene polymorphisms and chronic obstructive pulmonary disease in the Chinese Han population.The Journal of international medical research · 2020Article
- Stromal cells maintain immune cell homeostasis in adipose tissue via production of interleukin-33.Science immunology · 2019Article
- The interplay of type 2 immunity, helminth infection and the microbiota in regulating metabolism.Clinical & translational immunology · 2019Review
- Interleukin-33 in Systemic Sclerosis: Expression and Pathogenesis.Frontiers in immunology · 2018Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe effect of interleukin 33 (IL-33) in the inflammatory process generates significant interest in the potential significance of IL-33 as a biomarker for coronary artery disease (CAD). Here, our objective was to analyze whether IL-33 gene polymorphisms are associated with premature CAD in a case-control association study.
methodsFour IL-33 polymorphisms (rs7848215, rs16924144, rs16924159 and rs7044343) were genotyped by 5' exonuclease TaqMan assays in 1095 patients with premature CAD and 1118 controls.
resultsThe rs7044343 T allele was significantly associated with a diminished risk of premature CAD (OR = 0.81, 95% CI: 0.69-0.97, Pdom = 0.020; OR = 0.85, 95% CI: 0.75-0.96, Padd = 0.019) and central obesity (OR = 0.74, 95% CI: 0.58-0.93, Pdom = 0.0007), respectively. When patients were divided into groups with and without type 2 diabetes mellitus (T2DM), the rs7044343 T allele was associated with a reduced risk of premature CAD in patients without (OR = 0.85, 95% CI: 0.73-0.99, Padd = 0.038) and with T2DM (OR = 0.61, 95% CI: 0.38-0.97, Pdom = 0.039; OR = 0.69, 95% CI: 0.49-0.97, Padd = 0.035). In order to establish the functional effect of the rs7044343 polymorphism, the production of IL-33 was determined in monocytes of selected individuals. Monocytes from individuals with rs7044343 CC genotype produced higher levels of IL-33 than monocytes from individuals with other genotypes.
conclusionThe results suggest that the IL-33 rs7044343 T allele could be a susceptibility marker for premature CAD and central obesity. The rs7044343 polymorphism could be involved in regulating the production of IL-33.
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