ArticleFrontiers in cardiovascular medicine2022
Systemic lupus erythematosus and the risk of cardiovascular diseases: A two-sample Mendelian randomization study.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 8 citations in OpenAlex.
- Sleep Disorders and Nonalcoholic Fatty Liver Disease: Evidence From Meta-Analysis and Mendelian Randomization.Journal of prevention (2022) · 2026Pooled it
- Mendelian randomization studies on ischemic stroke: a field synopsis and systematic review.Journal of translational medicine · 2025Pooled it
- Combining Laboratory and Imaging Evaluation for Cardiovascular Risk Stratification in Systemic Lupus Erythematosus.Journal of clinical medicine · 2025Review
- Association between systemic lupus erythematosus and cardiovascular health based on genetic data.Clinical rheumatology · 2025Article
- Causal relationship between type II diabetes mellitus, metformin, insulin, gliclazide, and esophageal cancer-insights from two-sample Mendelian randomization study and meta-analysis.Journal of thoracic disease · 2025Article
- Causal association between common rheumatic diseases and arrhythmia: a Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Association between leptin and NAFLD: a two-sample Mendelian randomization study.European journal of medical research · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous observational studies have suggested that the causal role of systemic lupus erythematosus (SLE) in the risk of cardiovascular diseases (CVDs) remained inconsistent. In this study, we aimed to investigate the causal relationship between SLE and CVDs by two-sample Mendelian randomization (MR) analysis. Methods: Genetic instruments for SLE were obtained from a public genome-wide association study (GWAS) with 4,036 patients with SLE and 6,959 controls. Summary statistical data for CVDs, including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), ischemic stroke (IS), and its subtypes, were identified from other available GWAS meta-analyses. The inverse-variance weighted (IVW) method was used as the primary method to estimate the causal effect. The simple- and weighted-median method, MR-Egger method, and MR pleiotropy residual sum and outlier (MR-PRESSO) were provided as a supplement to the IVW method. Besides, we performed sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, to evaluate the robustness of the results. Results: A total of 15 single-nucleotide polymorphisms (SNPs) were identified after excluding linkage disequilibrium (LD) and potential confounding factors. According to the IVW results, our MR study indicated that genetically predicted SLE was not causally connected with the risk of CVDs [CAD: odds ratio (OR) = 1.005, 95% confidence interval (CI) = 0.986-1.024, Conclusion: Our two-sample MR analysis provided no evidence that genetically determined SLE was causally associated with the risk of CVDs.
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