ArticleCell reports. Medicine2022
Mendelian randomization and pathway analysis demonstrate shared genetic associations between lupus and coronary artery disease.
Article in Cell reports. Medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Early SLE may follow a fast comorbidity/multimorbidity trajectory associated with flare burden and glucocorticoid exposure.RMD open · 2026Article
- Article
- Combining Laboratory and Imaging Evaluation for Cardiovascular Risk Stratification in Systemic Lupus Erythematosus.Journal of clinical medicine · 2025Review
- A deep learning system for detecting systemic lupus erythematosus from retinal images.Cell reports. Medicine · 2025Article
- Association between systemic lupus erythematosus and cardiovascular health based on genetic data.Clinical rheumatology · 2025Article
- Distinct pathway-based effects of blood pressure and body mass index on cardiovascular traits: comparison of novel Mendelian randomization approaches.Genome medicine · 2025Article
- The causal relationship between thyroid dysfunction and carpal tunnel syndrome: A Mendelian randomization study.Medicine · 2025Article
- The effects of saturated and unsaturated fatty acids on MASLD: a Mendelian randomization analysis and in vivo experiment.European journal of nutrition · 2024Article
- Genetic association with autoimmune diseases identifies molecular mechanisms of coronary artery disease.iScience · 2024Article
- Disentangling the riddle of systemic lupus erythematosus with antiphospholipid syndrome: blood transcriptome analysis reveals a less-pronounced IFN-signature and distinct molecular profiles in venous versus arterial events.Annals of the rheumatic diseases · 2024Article
- Genetic overlap and Mendelian randomization analysis highlighted the causal relationship between psoriatic disease and migraine.Archives of dermatological research · 2024Article
- Examination of the shared genetic architecture between multiple sclerosis and systemic lupus erythematosus facilitates discovery of novel lupus risk loci.Human genetics · 2024Article
- METTL14-mediated N6-methyladenosine modification induces the ferroptosis of hypoxia/reoxygenation-induced cardiomyocytes.Journal of cardiothoracic surgery · 2024Article
- Causal relationship between psychological factors and hepatocellular carcinoma as revealed by Mendelian randomization.Journal of cancer research and clinical oncology · 2024Article
- Does epigenetic markers of HLA gene show association with coronary artery disease in Indian subjects?Molecular biology reports · 2024Article
- Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization.Journal of clinical medicine · 2024Article
- Impact of systemic lupus erythematosus on cardiovascular morphologic and functional phenotypes: a Mendelian randomization analysis.Frontiers in cardiovascular medicine · 2024Article
- Pathological mechanisms and crosstalk among various cell death pathways in cardiac involvement of systemic lupus erythematosus.Frontiers in immunology · 2024Review
- Molecular pathways identified from single nucleotide polymorphisms demonstrate mechanistic differences in systemic lupus erythematosus patients of Asian and European ancestry.Scientific reports · 2023Article
- Commentary: Systemic lupus erythematosus and cardiovascular disease: A Mendelian randomization study.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary artery disease (CAD) is a leading cause of death in patients with systemic lupus erythematosus (SLE). Despite clinical evidence supporting an association between SLE and CAD, pleiotropy-adjusted genetic association studies are limited and focus on only a few common risk loci. Here, we identify a net positive causal estimate of SLE-associated non-HLA SNPs on CAD by traditional Mendelian randomization (MR) approaches. Pathway analysis using SNP-to-gene mapping followed by unsupervised clustering based on protein-protein interactions (PPIs) identifies biological networks composed of positive and negative causal sets of genes. In addition, we confirm the casual effects of specific SNP-to-gene modules on CAD using only SNP mapping to each PPI-defined functional gene set as instrumental variables. This PPI-based MR approach elucidates various molecular pathways with causal implications between SLE and CAD and identifies biological pathways likely causative of both pathologies, revealing known and novel therapeutic interventions for managing CAD in SLE.
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