ArticleJournal of clinical laboratory analysis2022
Effects of IL-32 polymorphisms and IL-32 levels on the susceptibility and severity of coronary artery disease.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- The Emerging Role of Interleukin-32 in HIV-Associated Cardiovascular Comorbidities: A Mini Review.International journal of general medicine · 2026Review
- IL-32 as a potential biomarker and therapeutic target in cardiovascular disease.Frontiers in immunology · 2026Review
- Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease.Current cardiology reviews · 2025Review
- Circulating Interlukin-32 and Altered Blood Pressure Control in Individuals with Metabolic Dysfunction.International journal of molecular sciences · 2023Article
- Effects of IL-32 polymorphisms and IL-32 levels on the susceptibility and severity of coronary artery disease.Journal of clinical laboratory analysis · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInterleukin-32 (IL-32) has long been proposed as a biomarker for coronary artery disease (CAD). We aimed to evaluate the association between IL-32 levels and coronary stenosis severity, IL-32 polymorphisms rs28372698 and rs4786370, and CAD susceptibility.
methodsA total of 362 patients with definite or suspected CAD that underwent angiography were recruited (CAD group, n = 175; nonobstructive CAD group, n = 56; control group, n = 131). The severity of coronary stenosis was assessed using the Gensini score and the number of diseased vessels. IL-32 levels were determined using enzyme-linked immunosorbent assay. Gene polymorphisms were genotyped using PCR and sequencing techniques.
resultsIL-32 levels were significantly different at different levels of coronary artery stenosis (p < 0.05), and logIL-32 was positively correlated with the Gensini score (r = 0.357, p < 0.01). Multivariate logistic regression analysis revealed that IL-32 was independently associated with CAD (OR = 6.526, 95% CI: 3.344-12.739, p < 0.01). The receiver operating characteristic analysis revealed the area under the curve for discriminating the CAD and Gensini score were 0.605 and 0.613, respectively. Furthermore, IL-32 levels were significantly higher before percutaneous coronary intervention (PCI) than at 7 days post-PCI (p = 0.012). The homozygous TT genotype and T allele of rs28372698 were found to be associated with increased risk of CAD, while TT homozygosity and the T allele of rs4786370 with reduced risk of CAD (p < 0.05). However, both SNPs had no obvious effect on IL-32 levels or coronary stenosis severity in patients with CAD.
conclusionTo the best of our knowledge, our study is the first to show that rs28372698 and rs4786370 are associated with CAD susceptibility in Chinese Han population. We also suggest that plasma IL-32 levels may be indicative of coronary artery stenosis and the efficacy of PCI and provide guidance for risk stratification and disease management.
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