ArticleImmunology2020
Mendelian randomization analysis revealed potential causal factors for systemic lupus erythematosus.
Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Study on the causality of cathepsin on autoimmune diseases and cancer: evidence from mendelian randomization analysis.Archives of dermatological research · 2024Pooled it
- Shared genetic architecture of schizophrenia and lupus identifies pleiotropic loci with distinct downstream mechanisms.Human molecular genetics · 2026Article
- Screen Time and Chronic Pain Health: Mendelian Randomization Study.Journal of medical Internet research · 2026Article
- Integrative multi-omics and single-cell transcriptomics reveal ARHGEF12 driving chemoresistance in bladder cancer.Hereditas · 2025Article
- Integrated analyses of Mendelian randomization, eQTL, and single-cell transcriptome identify CCN3 as a potential biomarker in aortic dissection.Scientific reports · 2024Article
- Exploring Pathogenic Genes in Frozen Shoulder through weighted gene co-expression network analysis and Mendelian Randomization.International journal of medical sciences · 2024Article
- Association between copper intake and essential hypertension: dual evidence from Mendelian randomization analysis and the NHANES database.Frontiers in nutrition · 2024Article
- Spatial proteomics landscape and immune signature analysis of renal sample of lupus nephritis based on laser-captured microsection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Exploring genes for immunoglobulin A nephropathy: a summary data-based mendelian randomization and FUMA analysis.BMC medical genomics · 2023Article
- High throughput sequencing revealed enhanced cell cycle signaling in SLE patients.Scientific reports · 2023Article
- Modeling of horizontal pleiotropy identifies possible causal gene expression in systemic lupus erythematosus.Frontiers in lupus · 2023Article
- Mendelian randomization study on the causal effects of systemic lupus erythematosus on major depressive disorder.Journal of human genetics · 2023Article
- Article
- A transcriptome-wide association study provides new insights into the etiology of osteoarthritis.Annals of translational medicine · 2022Article
- Single cell sequencing analysis identifies genetics-modulated ORMDL3Journal of nanobiotechnology · 2021Article
- The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases.International journal of molecular sciences · 2021Review
- Mendelian randomization integrating GWAS and eQTL data revealed genes pleiotropically associated with major depressive disorder.Translational psychiatry · 2021Article
- A catalog of GWAS fine-mapping efforts in autoimmune disease.American journal of human genetics · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have identified many loci for systemic lupus erythematosus (SLE). However, identification of functionally relevant genes remains a challenge. The aim of this study was to highlight potential causal genes for SLE in the GWAS loci. By applying Mendelian randomization (MR) methods, such as summary data-based MR (SMR), generalized SMR and MR pleiotropy residual sum and outlier, we identified DNA methylations in 15 loci and mRNA expression of 21 genes that were causally associated with SLE. The identified genes enriched in 14 specific KEGG pathways (e.g. SLE, viral carcinogenesis) and two GO terms (interferon-γ-mediated signaling pathway and innate immune response). Among the identified genes, UBE2L3 and BLK variants were significantly associated with UBE2L3 and BLK methylations and gene expressions, respectively. UBE2L3 was up-regulated in SLE patients in several types of immune cells. Methylations (e.g. cg06850285) and mRNA expression of UBE2L3 were causally associated with SLE. Methylation site cg09528494 and mRNA expression of BLK were causally associated with SLE. BLK single nucleotide polymorphisms that were significantly associated with SLE were strongly associated with plasma cathepsin B level. Deep analysis identified that plasma cathepsin B level was causally associated with SLE. In summary, this study identified hundreds of DNA methylations and genes as potential risk factors for SLE. Genetic variants in UBE2L3 gene might affect SLE by influencing gene expression. Genetic variants in BLK gene might affect SLE by influencing BLK gene expression and plasma cathepsin B protein level.
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