ArticleThe journal of headache and pain2025
Causal proteomic insights into drug target discovery for tension-type headache.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- SMR Analysis Integrating GWAS and eQTL Data Reveals UHRF1BP1 and SNRPC as Potential Drug Targets for Low Back Pain.Journal of pain research · 2026Article
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3 authors.
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Abstract
backgroundThe pathophysiology of tension-type headache (TTH) remains poorly understood, and current treatments are largely symptomatic. Identifying genetically supported, causally relevant proteins may provide insights into disease mechanisms and enable precision therapeutics.
methodsWe conducted a proteome-wide Mendelian randomization (MR) analysis integrating large-scale plasma proteomic quantitative trait loci with genome-wide association study data for TTH. Phenome-wide MR, enrichment, protein-protein interaction (PPI), and mediation analyses were performed to identify druggable targets and clarify potential biological pathways.
resultsThirteen plasma proteins exhibited significant causal associations with TTH (Bonferroni correction p < 2.76 × 10− 5). Enrichment analysis revealed ensheathment of neurons and cellular response to cholesterol and sterol as key pathways. Mediation analyses identified 3-methylglutaconate and 3-hydroxydecanoate as partial mediators of the proteomic effects on TTH, reflecting mitochondrial leucine catabolism and mitochondrial fatty acid beta oxidation, with mediation proportions of 7.5% to 15.2%. Phenome-wide MR analysis indicated that NRXN3, CCL22, CLEC1B, and LRIG1 were not associated with any major adverse effects. PPI analysis further showed that these proteins are functionally connected to proteins targeted by current TTH therapies, supporting their safety and translational potential.
conclusionsThis integrative genetic analysis identified multiple plasma proteins with causal and pharmacologically relevant roles in NRXN3, CCL22, CLEC1B, and LRIG1 emerged as promising and potentially safe therapeutic targets.
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