ArticleJournal of cellular and molecular medicine2025
Integrating Genomic, eQTL, and Mendelian Randomization Analyses to Identify Microglial Drug Targets in Multiple Sclerosis.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Integrating Genomic, eQTL, and Mendelian Randomization Analyses to Identify Microglial Drug Targets in Multiple Sclerosis.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune disease characterised by neuroinflammation and neurodegeneration. This study investigates genetic and immunological factors in MS, focusing on microglial regulation. We analysed differentially expressed genes using RNA sequencing from MS lesions (GSE108000) and plaques (GSE227781), validated with cis-eQTL analysis, and integrated Mendelian randomisation (MR), SMR, co-localisation, methylation, and protein-protein interaction (PPI) analyses to assess causal effects on MS risk. We identified five genes-ARHGAP25, HLA-DRB1, MERTK, MS4A6A, and SYK-linked to MS susceptibility. MR revealed that elevated levels of ARHGAP25 (OR = 1.45), HLA-DRB1 (OR = 2.24), MERTK (OR = 1.10), MS4A6A (OR = 1.15), and SYK (OR = 1.13) increased MS risk. SMR confirmed a causal link between HLA-DRB1 and MS, while co-localisation analysis showed shared variants with MS for HLA-DRB1 (100%) and SYK (97.93%). Methylation analysis highlighted 10 sites within HLA-DRB1, and PPI and DrugBank analyses revealed interactions between these genes and multiple proteins or chemicals. This study demonstrates the value of integrating genomic and eQTL data through MR to identify novel MS therapeutic targets, particularly microglial genes, offering potential new avenues for treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.