Identification of Potential Differentially Methylated Gene-Related Biomarkers in Endometriosis

Epigenomics · 2022 · vol. 14(19) , pp. 1157–1179 · doi:10.2217/epi-2022-0249 · PMID:36314280 · W4307770862
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AI-generated summary by claude@2026-06, 2026-06-07

This study identified BDNF and CCL2 as key DNA methylation-driven genes in endometriosis development and flagged four chemical agents as potential therapeutic targets.

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Abstract

Aim: To identify epigenetic alterations of differentially expressed genes and screen out targeted therapeutic drugs in endometriosis. Methods: Based on the Gene Expression Omnibus database and a series of biological information analysis tools, supplemented by validation of clinical samples, aberrant DNA methylation-driven genes and their functions were explored, as well as possible targeted drugs. Results: This study screened out a range of DNA methylation-driven genes that were associated with powerful properties and corresponding pathways. Among them, BDNF and CCL2 were key genes in the development of endometriosis. Four chemical agents have been flagged as potential treatments for endometriosis. Conclusion: These candidate genes and small-molecule agents may be further explored as potential targets and drugs for endometriosis diagnosis and therapy, respectively.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis DNA Methylation DNA Methylation

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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