Evidence map›Paper›PMID 33376509›Full record

ArticleExperimental and therapeutic medicine2021

Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32.

Urban Alehagen, Levar Shamoun, Jan Ingvar Dimberg, Dick Wågsäter

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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0cells of the map it votes in
3citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Urban AlehagenDivision of Cardiovascular Medicine, Department of Medicine and Health Sciences, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden.
Levar ShamounDivision of Medical Diagnostics, Department of Laboratory Medicine, Jönköping County, SE-553 05 Jönköping, Sweden.
Jan Ingvar DimbergDepartment of Natural Science and Biomedicine, School of Health and Welfare, Jönköping University, SE-553 18 Jönköping, Sweden.
Dick WågsäterDepartment of Medical Cell Biology, Uppsala University, SE-752 36 Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the major causes of mortality in the western hemisphere is cardiovascular disease. Therefore, a variety of markers to identify those at risk are required. Interleukin-32 (IL-32) is a cytokine that is associated with inflammation. The aim of the current study was to investigate variations in single nucleotide polymorphisms (SNPs) of IL-32 and plasma expression, and their associations with mortality. A population of 486 elderly community-living persons were evaluated. The participants were followed for 7.1 years and underwent a clinical examination and blood sampling. SNP analyses of IL-32 rs28372698 using allelic discrimination and plasma measurement of IL-32, using ELISA, were performed. During the follow-up period, 140 (28.8%) all-cause and 87 (17.9%) cardiovascular deaths were registered. No significant difference between mortality and plasma concentration of IL-32 was observed. The A/A genotype group exhibited significantly higher all-cause mortality (P=0.036), and an almost two-fold increased risk in a multivariate Cox regression model for all-cause and cardiovascular mortality. A highly significant difference in all-cause and cardiovascular mortality between the A/A and the T/T groups was demonstrated (P=0.015 resp. P=0.014). In the present study, the cytokine IL-32 was demonstrated to have prognostic information, with an increased risk of all-cause and cardiovascular mortality for those with the A/A genotype rs28372698 of IL-32. The A/A genotype could therefore be regarded as a possible biomarker for mortality risk that may be used to offer optimized cardiovascular patient handling in the future. However, the present study sample was small, and the results should be regarded as hypothesis-generating.

Indexed as

genotypesinterleukin-32mortality

Identifiers

PMID33376509
PMCPMC7751449

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