ArticleScientific reports2025
Multiomic insight into the involvement of cell aging related genes in the pathogenesis of endometriosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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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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.
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Who cites it
7 citing papers in PubMed.
- p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Translational Assessment of Omics Approaches in Endometriosis: Bridging Molecular Discovery with Clinical Utility.International journal of molecular sciences · 2026Review
- Advances in multi-omics and aging clock research for female reproductive health and aging.MedScience · 2026Review
- Multi-omics Mendelian randomization integrating metabolism, microbiome and immunity supports a putative gut-immune-pelvic pathway in deep infiltrating endometriosis.Frontiers in endocrinology · 2026Article
- The Nexus of Iron, Senescence, and Fibrosis in Endometriosis: A Narrative Review.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- The emerging role of multiomics in aging research.Epigenomics · 2025Review
- Identification of Potential Oxidative Stress-Related Causal Genes for Calculus of Kidney and Ureter: A Multi-Omics Mendelian Randomization Analysis.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Endometriosis significantly impacts women's health and fertility, with cell aging playing a crucial role in its development. This study utilized a multi-omic summary Mendelian randomization (SMR) analysis, integrating genome-wide association studies (GWAS), expression quantitative trait loci (eQTLs), methylation quantitative trait loci (mQTLs), and protein quantitative trait loci (pQTLs). The goal was to identify genes that exhibit causal associations between cell aging and endometriosis. Validation was conducted using the FinnGen R10 and UK Biobank cohorts. The SMR and HEIDI tests evaluated the genetic variants linked to both cell aging and endometriosis risk. Colocalization analysis revealed shared genetic variants, uncovering significant associations between the two conditions. A total of 196 CpG sites in 78 genes, alongside 18 eQTL-associated genes and 7 pQTL-associated proteins, were identified. Notably, the MAP3K5 gene displayed contrasting methylation patterns linked to endometriosis risk. In validation cohorts, the THRB gene and ENG protein were confirmed as risk factors. The findings suggest a causal mechanism where specific methylation patterns downregulate the MAP3K5 gene, heightening endometriosis risk, highlighting it and associated pathways as potential therapeutic targets.
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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.