Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities

Yishen S. Rong, Rong YS, Zhu J, Jue Zhu, Wang CC, Chi Chiu Wang, Zhang J, Jing Zhang, Yichen C Chen, Chen YC, Yichen Chen, Yuehua Chen
iScience · 2026 · vol. 29(6) , pp. 115916 · doi:10.1016/j.isci.2026.115916 · PMID:42291235 · W7163152246
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-06 ⓘ

This review examines how mitochondrial dysfunction contributes to endometriosis progression through metabolic changes and oxidative stress, and discusses potential therapeutic strategies targeting these mechanisms.

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Abstract

Endometriosis affects about 10% of women of reproductive age and is a major cause of chronic pelvic pain and infertility, yet current therapies often fail to provide lasting relief. Mitochondrial dysfunction has emerged as a potential key contributor that drives disease progression through metabolic reprogramming, oxidative stress (OS), and mitochondrial DNA (mtDNA) abnormalities. These alterations disrupt energy metabolism, promote ectopic cell survival under hypoxia, and increase oxidative damage. This review highlights mitochondrial failure as both a proposed driver and therapeutic target, discussing biomarkers and emerging interventions including antioxidants, metabolic modulation, oxidative phosphorylation (OXPHOS) inhibition, and bioactive substances.

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Condition tags

endometriosischronic_pelvic_paininfertility

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.

References (100)

Cited by (1)

SciLite annotations

organisms 1
noordeloos 2009062
chemicals 10
tricarboxylic acid oxygen glutathione vitamin c iron iron iron iron aldehyde iron

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