Redox-Survival Mechanisms in Endometriosis: Public Transcriptomic Analysis and Mechanistic Framework

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⚙ AI-generated summary by qwen3.7-flash, 2026-10-14 ⓘ

This mechanistic framework examined selective redox regulation in endometriosis and adenomyosis using public transcriptomic data, finding partial context-dependent transcriptional organization but no evidence for antioxidant capacity or survival advantage.

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Abstract

This project contains the public transcriptomic analyses and reproducibility materials for a mechanistic framework examining selective redox regulation in endometriosis and adenomyosis. The hypothesis-directed benchmark combines complementary tissue comparisons and donor-level cell-population analyses; it is not an exhaustive systematic review. The current manuscript is “Redox Regulation as a Candidate Survival Mechanism in Endometriosis Establishment” by Jonathon Castillo. The release contains the manuscript, supplementary methods and information, a 71-sheet results workbook, figures and source data, analytical scripts, processed inputs, provenance and a SHA-256 file manifest. Download Redox Regulation in Endometriosis - OSF Release.zip for the complete research package; the separately listed manuscript and supplements are convenience copies of the same release. The findings support partial context-dependent transcriptional organization, while retaining null, contradictory and non-testable results. The external GSE266265 eutopic cohort was predominantly null under the primary redox tests. GSE193928 contributes technical QC only, GSE74373 is gene-level non-testable, and GSE7305 is tissue-mixed sensitivity evidence. Transcriptomic associations do not establish antioxidant capacity, survival advantage, causality, treatment efficacy or clinical validation. Dataset prioritization and the limits of the retained historical candidate-disposition record are documented in Supplementary Methods. CC BY 4.0 applies to author-created materials. Third-party data and source materials remain subject to their original rights and licenses; their inclusion does not relicense them. This research received no external or commercial funding and was conducted independently by the author.

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last seen: 2026-10-13T06:02:51.577429+00:00
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