Redox Regulation as a Candidate Survival Mechanism in Endometriosis Establishment

Endometrial-like tissue can establish persistent lesions outside its usual environment, but anatomical explanations for its arrival leave a second question unresolved: what permits survival during establishment? We evaluated a pre-existing selective redox-survival hypothesis using 27 historical transcriptomic comparisons across six accessions and an external donor-level analysis of proliferative eutopic endometrium from 12 endometriosis cases and 11 clinical controls. TXN reduction and ovarian ferritin/metabolic changes recurred across specified historical lesion cohorts. Historical mean survival-module shifts were null after across-test correction. The conservative expanded nondirectional sensitivity family retained eight historical but no external survival-associated sets. No external primary panel gene or population interaction met its declared threshold; limited overlapping HIF-set signals did not pass external-only correction. A later secondary test of paired peritoneal/eutopic responses found that held-out donors resembled their own cellular context more than other contexts: similarity margin 0.298, permutation P=0.0001, with 69.0% classification accuracy versus 16.7% chance. This used seven donors, six non-overlapping populations and 43 shared frozen-panel genes. Convergence varied by population and did not clearly exceed expression-matched background sets (empirical P=0.0939). The results support partial context constraint with substantial patient flexibility, while narrowing extrapolation to a common eutopic survival state. They do not establish redox-specific protection, early survival advantage, intercellular rescue or a receptor/proteoform mechanism. The central causal proposition remains unresolved.