ArticleMolecular neurobiology2025
Systematic Mendelian Randomization Exploring Druggable Genes for Hemorrhagic Strokes.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integration of Genome-Wide Association Studies With Single-Cell and Bulk Expression Quantitative Trait Locus to Identify Stroke Susceptibility Genes.Journal of the American Heart Association · 2026Article
- Mendelian Randomization Study on Serum Metabolites and Diabetic Nephropathy Risk: Identifying Potential Biomarkers for Early Intervention.Current pharmaceutical design · 2026Article
- Druggable genome-wide Mendelian randomization integrating GWAS and eQTL/pQTL data identifies targets for lung squamous cell carcinoma.Scientific reports · 2025Article
- Multi-Omic Insight Into the Molecular Networks in the Pathogenesis of Coronary Artery Disease.Journal of the American Heart Association · 2025Article
- Druggable genome-wide Mendelian randomization analysis identifies potential treatment targets in vascular dementia.Alzheimer's & dementia (New York, N. Y.)Article
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Authors and funding
7 authors.
Funding
Abstract
Patients with hemorrhagic stroke have high rates of morbidity and mortality, and drugs for prevention are very limited. Mendelian randomization (MR) analysis can increase the success rate of drug development by providing genetic evidence. Previous MR analyses only analyzed the role of individual drug target genes in hemorrhagic stroke; therefore, we used MR analysis to systematically explore the druggable genes for hemorrhagic stroke. We sequentially performed summary-data-based MR analysis and two-sample MR analysis to assess the associations of all genes within the database with intracranial aneurysm, intracerebral hemorrhage, and their subtypes. Validated genes were further analyzed by colocalization. Only genes that were positive in all three analyses and were druggable were considered desirable genes. We also explored the mediators of genes affecting hemorrhagic stroke incidence. Finally, the associations of druggable genes with other cardiovascular diseases were analyzed to assess potential side effects. We identified 56 genes that significantly affected hemorrhagic stroke incidence. Moreover, TNFSF12, SLC22A4, SPARC, KL, RELT, and ADORA3 were found to be druggable. The inhibition of TNFSF12, SLC22A4, and SPARC can reduce the risk of intracranial aneurysm, subarachnoid hemorrhage, and intracerebral hemorrhage. Gene-induced hypertension may be a potential mechanism by which these genes cause hemorrhagic stroke. We also found that blocking these genes may cause side effects, such as ischemic stroke and its subtypes. Our study revealed that six druggable genes were associated with hemorrhagic stroke, and the inhibition of TNFSF12, SLC22A4, and SPARC had preventive effects against hemorrhagic strokes.
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