Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study
BackgroundPrevious studies have shown that patients with systemic lupus erythematosus (SLE) tend to have a higher risk of cardiovascular disease (CVD), but the potential causal relationship between genetic susceptibility to SLE and CVD risk is not clear. This study systematically investigated the po...
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Frontiers Media S.A.
2022-06-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.908831/full |
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author | Ning Gao Minjian Kong Xuebiao Li Dongdong Wei Xian Zhu Ze Hong Ming Ni Yifan Wang Aiqiang Dong |
author_facet | Ning Gao Minjian Kong Xuebiao Li Dongdong Wei Xian Zhu Ze Hong Ming Ni Yifan Wang Aiqiang Dong |
author_sort | Ning Gao |
collection | DOAJ |
description | BackgroundPrevious studies have shown that patients with systemic lupus erythematosus (SLE) tend to have a higher risk of cardiovascular disease (CVD), but the potential causal relationship between genetic susceptibility to SLE and CVD risk is not clear. This study systematically investigated the potential association between genetically determined SLE and the risk of CVD.MethodsThe genetic tools were obtained from genome-wide association studies of SLE and CVD, with no overlap between their participating populations. Mendelian randomization (MR) analysis was performed using inverse variance weighting as the primary method. Simultaneously, a series of repeated analyses, sensitivity analyses, and instrumental variable strength evaluations were performed to verify the reliability of our results.ResultsMR analysis showed that genetic susceptibility to SLE was associated with a higher risk of heart failure (OR=1.025, 95% CI [1.009-1.041], P=0.002), ischemic stroke (OR=1.020, 95% CI [1.005-1.034], P=0.009), and venous thromboembolism (OR=1.001, 95% CI [1.000-1.002], P=0.014). However, genetic susceptibility to SLE was negatively correlated with the risk of type 2 diabetes (OR=0.968, 95% CI [0.947-0.990], P=0.004). Sensitivity analysis found no evidence of horizontal pleiotropy or heterogeneity.ConclusionOur MR study explored the causal role of SLE in the etiology of CVD, which would help improve our understanding of the basic disease mechanisms of SLE and provide comprehensive CVD assessment and treatment for SLE patients. |
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issn | 1664-3224 |
language | English |
last_indexed | 2024-04-12T14:25:50Z |
publishDate | 2022-06-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Immunology |
spelling | doaj.art-ff6233095b08475ba4a3470940c325ca2022-12-22T03:29:27ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-06-011310.3389/fimmu.2022.908831908831Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization StudyNing GaoMinjian KongXuebiao LiDongdong WeiXian ZhuZe HongMing NiYifan WangAiqiang DongBackgroundPrevious studies have shown that patients with systemic lupus erythematosus (SLE) tend to have a higher risk of cardiovascular disease (CVD), but the potential causal relationship between genetic susceptibility to SLE and CVD risk is not clear. This study systematically investigated the potential association between genetically determined SLE and the risk of CVD.MethodsThe genetic tools were obtained from genome-wide association studies of SLE and CVD, with no overlap between their participating populations. Mendelian randomization (MR) analysis was performed using inverse variance weighting as the primary method. Simultaneously, a series of repeated analyses, sensitivity analyses, and instrumental variable strength evaluations were performed to verify the reliability of our results.ResultsMR analysis showed that genetic susceptibility to SLE was associated with a higher risk of heart failure (OR=1.025, 95% CI [1.009-1.041], P=0.002), ischemic stroke (OR=1.020, 95% CI [1.005-1.034], P=0.009), and venous thromboembolism (OR=1.001, 95% CI [1.000-1.002], P=0.014). However, genetic susceptibility to SLE was negatively correlated with the risk of type 2 diabetes (OR=0.968, 95% CI [0.947-0.990], P=0.004). Sensitivity analysis found no evidence of horizontal pleiotropy or heterogeneity.ConclusionOur MR study explored the causal role of SLE in the etiology of CVD, which would help improve our understanding of the basic disease mechanisms of SLE and provide comprehensive CVD assessment and treatment for SLE patients.https://www.frontiersin.org/articles/10.3389/fimmu.2022.908831/fullsystemic lupus erythematosuscardiovascular diseaseMendelian randomizationthe causal linkgenome-wide association study |
spellingShingle | Ning Gao Minjian Kong Xuebiao Li Dongdong Wei Xian Zhu Ze Hong Ming Ni Yifan Wang Aiqiang Dong Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study Frontiers in Immunology systemic lupus erythematosus cardiovascular disease Mendelian randomization the causal link genome-wide association study |
title | Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study |
title_full | Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study |
title_fullStr | Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study |
title_full_unstemmed | Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study |
title_short | Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study |
title_sort | systemic lupus erythematosus and cardiovascular disease a mendelian randomization study |
topic | systemic lupus erythematosus cardiovascular disease Mendelian randomization the causal link genome-wide association study |
url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.908831/full |
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