The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research
We evaluated the causal effects of blood lipid levels on systemic lupus erythematosus with a two-sample Mendelian randomization analysis. Independent single-nucleotide polymorphisms related to blood lipids levels (<i>p</i> < 5 × 10<sup>−8</sup>) were selected as instrument...
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MDPI AG
2022-12-01
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| author | Yang Ding Shasha Fan Yi Tang Mengjiao He Mingyang Ren Yunjuan Shi Xiaohua Tao Wei Lu |
| author_facet | Yang Ding Shasha Fan Yi Tang Mengjiao He Mingyang Ren Yunjuan Shi Xiaohua Tao Wei Lu |
| author_sort | Yang Ding |
| collection | DOAJ |
| description | We evaluated the causal effects of blood lipid levels on systemic lupus erythematosus with a two-sample Mendelian randomization analysis. Independent single-nucleotide polymorphisms related to blood lipids levels (<i>p</i> < 5 × 10<sup>−8</sup>) were selected as instrumental variables (IVs) from a published genome-wide association study (GWAS). SLE GWAS analysis that included 4036 cases and 6959 controls of European ancestry provided the related roles between instrumental variables and result (SLE). The causal effects were evaluated with two-sample Mendelian randomization (MR) analyses. According to the inverse-variance weighted approaches, genes predictive of increased LDL cholesterol (OR: 1.131; 95% CI: 0.838, 1.528; <i>p</i> = 0.420), HDL cholesterol (OR: 1.093; 95% CI: 0.884, 1.352; <i>p</i> = 0.412), triglycerides (OR: 0.903; 95% CI: 0.716, 1.137; <i>p</i> = 0.384), Apolipoprotein A-I (OR: 0.854; 95% CI: 0.680, 1.074; <i>p</i> = 0.177), and Apolipoprotein B (OR: 0.933; 95% CI: 0.719, 1.211; <i>p</i> = 0.605) were not causally related to the risk of SLE, consistent with multivariate Mendelian randomization analysis. The reverse-MR analyses showed no massive causal roles between SLE and LDL cholesterol (OR: 0.998; 95% CI: 0.994, 1.001; <i>p</i> = 0.166) as well as Apolipoprotein B (OR: 0.998; 95% CI: 0.994, 1.001; <i>p</i> = 0.229). Nevertheless, a causal role of SLE in decreasing HDL cholesterol (OR: 0.993; 95% CI: 0.988, 0.997; <i>p</i> = 0.002), triglycerides (OR: 0.996; 95% CI: 0.993, 0.999; <i>p</i> = 0.010), and Apolipoprotein A-I (OR: 0.995; 95% CI: 0.990, 0.999; <i>p</i> = 0.026) was validated to some extent. Our study found no causal association between abnormal blood lipids and SLE nor a causal effect between SLE and LDL cholesterol as well as Apolipoprotein B. Nevertheless, some evidence showed that SLE exerted a causal effect on lowering HDL cholesterol, Apolipoprotein A-I, and triglyceride levels. |
| first_indexed | 2024-03-09T11:43:49Z |
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| language | English |
| last_indexed | 2024-03-09T11:43:49Z |
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| spelling | doaj.art-b91b9ccc90d2483fa09ab24a16ad495e2023-11-30T23:27:49ZengMDPI AGMetabolites2218-19892022-12-011312710.3390/metabo13010027The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization ResearchYang Ding0Shasha Fan1Yi Tang2Mengjiao He3Mingyang Ren4Yunjuan Shi5Xiaohua Tao6Wei Lu7Health Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaHealth Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaHealth Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaDepartments of Environmental Health, School of Public Health, Hangzhou Normal University, Hangzhou 310009, ChinaHealth Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaGraduate School of Bengbu Medical College, Bengbu 233030, ChinaHealth Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaHealth Management Center, Department of Dermatology, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital of Hangzhou Medical College, No. 158, Shangtang Road, Hangzhou 310014, ChinaWe evaluated the causal effects of blood lipid levels on systemic lupus erythematosus with a two-sample Mendelian randomization analysis. Independent single-nucleotide polymorphisms related to blood lipids levels (<i>p</i> < 5 × 10<sup>−8</sup>) were selected as instrumental variables (IVs) from a published genome-wide association study (GWAS). SLE GWAS analysis that included 4036 cases and 6959 controls of European ancestry provided the related roles between instrumental variables and result (SLE). The causal effects were evaluated with two-sample Mendelian randomization (MR) analyses. According to the inverse-variance weighted approaches, genes predictive of increased LDL cholesterol (OR: 1.131; 95% CI: 0.838, 1.528; <i>p</i> = 0.420), HDL cholesterol (OR: 1.093; 95% CI: 0.884, 1.352; <i>p</i> = 0.412), triglycerides (OR: 0.903; 95% CI: 0.716, 1.137; <i>p</i> = 0.384), Apolipoprotein A-I (OR: 0.854; 95% CI: 0.680, 1.074; <i>p</i> = 0.177), and Apolipoprotein B (OR: 0.933; 95% CI: 0.719, 1.211; <i>p</i> = 0.605) were not causally related to the risk of SLE, consistent with multivariate Mendelian randomization analysis. The reverse-MR analyses showed no massive causal roles between SLE and LDL cholesterol (OR: 0.998; 95% CI: 0.994, 1.001; <i>p</i> = 0.166) as well as Apolipoprotein B (OR: 0.998; 95% CI: 0.994, 1.001; <i>p</i> = 0.229). Nevertheless, a causal role of SLE in decreasing HDL cholesterol (OR: 0.993; 95% CI: 0.988, 0.997; <i>p</i> = 0.002), triglycerides (OR: 0.996; 95% CI: 0.993, 0.999; <i>p</i> = 0.010), and Apolipoprotein A-I (OR: 0.995; 95% CI: 0.990, 0.999; <i>p</i> = 0.026) was validated to some extent. Our study found no causal association between abnormal blood lipids and SLE nor a causal effect between SLE and LDL cholesterol as well as Apolipoprotein B. Nevertheless, some evidence showed that SLE exerted a causal effect on lowering HDL cholesterol, Apolipoprotein A-I, and triglyceride levels.https://www.mdpi.com/2218-1989/13/1/27blood lipidssystemic lupus erythematosusMendelian randomization |
| spellingShingle | Yang Ding Shasha Fan Yi Tang Mengjiao He Mingyang Ren Yunjuan Shi Xiaohua Tao Wei Lu The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research Metabolites blood lipids systemic lupus erythematosus Mendelian randomization |
| title | The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research |
| title_full | The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research |
| title_fullStr | The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research |
| title_full_unstemmed | The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research |
| title_short | The Association between Blood Lipids and Systemic Lupus Erythematosus: A Two-Sample Mendelian Randomization Research |
| title_sort | association between blood lipids and systemic lupus erythematosus a two sample mendelian randomization research |
| topic | blood lipids systemic lupus erythematosus Mendelian randomization |
| url | https://www.mdpi.com/2218-1989/13/1/27 |
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