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Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction
BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide associat...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755576/ https://www.ncbi.nlm.nih.gov/pubmed/36532051 http://dx.doi.org/10.3389/fimmu.2022.1017444 |
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author | Guo, Hao-Yang Wang, Wei Peng, Hui Yuan, Hui |
author_facet | Guo, Hao-Yang Wang, Wei Peng, Hui Yuan, Hui |
author_sort | Guo, Hao-Yang |
collection | PubMed |
description | BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide association study summary datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using inverse-variance weighted (IVW), weighted median, MR-Egger regression, simple mode, and weighted mode methods. RESULTS: The MR results for the causal effect of RA on MI (IVW, odds ratio [OR] = 1.041, 95% confidence interval [CI]: 1.007–1.076, P = 0.017; weighted median, OR = 1.027, 95% CI: 1.006–1.049, P = 0.012) supported a causal association between genetic susceptibility to RA and an increased risk of MI. MR results for the causal effect of MI on RA (IVW, OR = 1.012, 95% CI: 0.807–1.268, P = 0.921; weighted median, OR = 1.069, 95% CI: 0.855–1.338, P = 0.556) indicated that there was no causal association between genetic susceptibility to MI and an increased risk of RA. CONCLUSION: Bidirectional TSMR analysis supports a causal association between genetic susceptibility to RA and an increased risk of MI but does not support a causal association between genetic susceptibility to MI and an increased risk of RA. |
format | Online Article Text |
id | pubmed-9755576 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-97555762022-12-17 Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction Guo, Hao-Yang Wang, Wei Peng, Hui Yuan, Hui Front Immunol Immunology BACKGROUND: Epidemiological evidence suggests an association between rheumatoid arthritis (RA) and myocardial infarction (MI). However, causality remains uncertain. Therefore, this study aimed to explore the causal association between RA and MI. METHODS: Using publicly available genome-wide association study summary datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using inverse-variance weighted (IVW), weighted median, MR-Egger regression, simple mode, and weighted mode methods. RESULTS: The MR results for the causal effect of RA on MI (IVW, odds ratio [OR] = 1.041, 95% confidence interval [CI]: 1.007–1.076, P = 0.017; weighted median, OR = 1.027, 95% CI: 1.006–1.049, P = 0.012) supported a causal association between genetic susceptibility to RA and an increased risk of MI. MR results for the causal effect of MI on RA (IVW, OR = 1.012, 95% CI: 0.807–1.268, P = 0.921; weighted median, OR = 1.069, 95% CI: 0.855–1.338, P = 0.556) indicated that there was no causal association between genetic susceptibility to MI and an increased risk of RA. CONCLUSION: Bidirectional TSMR analysis supports a causal association between genetic susceptibility to RA and an increased risk of MI but does not support a causal association between genetic susceptibility to MI and an increased risk of RA. Frontiers Media S.A. 2022-12-02 /pmc/articles/PMC9755576/ /pubmed/36532051 http://dx.doi.org/10.3389/fimmu.2022.1017444 Text en Copyright © 2022 Guo, Wang, Peng and Yuan https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Guo, Hao-Yang Wang, Wei Peng, Hui Yuan, Hui Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title | Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title_full | Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title_fullStr | Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title_full_unstemmed | Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title_short | Bidirectional two-sample Mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
title_sort | bidirectional two-sample mendelian randomization study of causality between rheumatoid arthritis and myocardial infarction |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755576/ https://www.ncbi.nlm.nih.gov/pubmed/36532051 http://dx.doi.org/10.3389/fimmu.2022.1017444 |
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