ArticleFrontiers in endocrinology2024
Identification of potential druggable targets for endometriosis through Mendelian randomization analysis.
Article in Frontiers in endocrinology, 2024. 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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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.
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Who cites it
1 citing paper in PubMed.
- New therapeutic targets for endometriosis predicted through mendelian randomization analysis and case-control trials.Frontiers in genetics · 2025Article
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6 authors.
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Abstract
Introduction: Endometriosis (EM) is a widely recognized disorder in gynecological endocrinology. Although hormonal therapies are frequently employed for EM, their side effects and outcome limitations underscore the need to explore the genetic basis and potential drug targets for developing innovative therapeutic approaches. This study aimed to identify both cerebrospinal fluid (CSF) and plasma protein markers as promising therapeutic targets for EM. Methods: We utilized Mendelian randomization (MR) analysis to explore potential disease-causing proteins, utilizing genetic datasets from genome-wide association studies (GWAS) and protein quantitative trait loci (pQTL) analyses. We applied a range of validation techniques, including reverse causality detection, phenotype scanning, Bayesian co-localization (BC) analysis, and external validations to substantiate our findings. Additionally, we conducted a protein-protein interaction (PPI) network as well as functional enrichment analyses to unveil potential associations among target proteins. Results: MR analysis revealed that a decrease of one standard deviation (SD) in plasma R-Spondin 3 (RSPO3) level had a protective effect on EM (OR = 1.0029; 95% confidence interval (95% CI): 1.0015-1.0043; P = 3.2567e-05; Bonferroni P < 5.63 × 10 Discussion: In conclusion, this comprehensive study offers valuable insights into potential drug targets for EM, with RSPO3 emerging as a promising candidate. Additionally, mechanistic roles of FN1, glycan degradation pathway, LGALS3, CPE, and FUT5 in EM warrant further investigation.
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