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Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32
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 s...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751449/ https://www.ncbi.nlm.nih.gov/pubmed/33376509 http://dx.doi.org/10.3892/etm.2020.9559 |
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author | Alehagen, Urban Shamoun, Levar Dimberg, Jan Ingvar Wågsäter, Dick |
author_facet | Alehagen, Urban Shamoun, Levar Dimberg, Jan Ingvar Wågsäter, Dick |
author_sort | Alehagen, Urban |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7751449 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-77514492020-12-28 Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 Alehagen, Urban Shamoun, Levar Dimberg, Jan Ingvar Wågsäter, Dick Exp Ther Med Articles 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. D.A. Spandidos 2021-02 2020-12-07 /pmc/articles/PMC7751449/ /pubmed/33376509 http://dx.doi.org/10.3892/etm.2020.9559 Text en Copyright: © Alehagen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Alehagen, Urban Shamoun, Levar Dimberg, Jan Ingvar Wågsäter, Dick Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title | Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title_full | Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title_fullStr | Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title_full_unstemmed | Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title_short | Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32 |
title_sort | increased mortality in the a/a genotype of the snp rs28372698 of interleukin 32 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751449/ https://www.ncbi.nlm.nih.gov/pubmed/33376509 http://dx.doi.org/10.3892/etm.2020.9559 |
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