Oxidative stress and endometriosis

Yeon Jean Cho, Heung Yeol Kim
In: Kosin Medical Journal · 2018 · vol. 33(2) , pp. 135–140 · doi:10.7180/kmj.2018.33.2.135 · W2908717138
article OA: diamond CC0 ⤵ 5 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This paper reviews recent findings on how oxidative stress, particularly iron-induced ROS, contributes to endometriosis development and progression by activating key signaling pathways and influencing epigenetic mechanisms.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a review examining how oxidative stress and reactive oxygen species contribute to the pathogenesis of endometriosis, integrating evidence from studies of peritoneal oxidative environments, iron-driven ROS generation, and downstream signaling. It summarizes mechanisms linking iron overload to ROS via the Fenton reaction, increased pro-inflammatory pathways such as NF-κB, and oxidative activation of ERK1/2 as well as PI3K/AKT/mTOR signaling that supports processes like lesion progression, adhesion, angiogenesis, and proliferation, while also discussing oxidative involvement in epigenetic mechanisms. A key limitation is that, as a narrative review, it does not present new original experiments or a systematic, quantified assessment of evidence strength across outcomes. This paper is centrally about endometriosis — it specifically reviews oxidative stress mechanisms (including ROS imbalance and iron-induced oxidative damage) in endometriosis pathophysiology.

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Abstract

Endometriosis is an estrogen-dependent chronic inflammatory condition that affects women in their reproductive period and is associated with pelvic pain and infertility. Oxidative stress (OS) occurs when reactive oxygen stress (ROS) and anti-oxidants are in imbalance. OS is a potential factor involved in the pathophysiology of endometriosis. Iron-induced ROS may trigger a chain of events resulting in the development and progression of endometriosis. Endogenous ROS are correlated with increased cellular proliferation and ERK1/2 activation in human endometriotic cells. An oxidative environment leads to stimulation of the ERK and PI3K/AKT/mTOR signaling pathways that facilitate endometriotic lesion progression through adhesion, angiogenesis, and proliferation. OS is also known to be involved in epigenetic mechanisms in endometriosis. We summarize the recent knowledge in our understanding of the role of oxidative stress in the pathogenesis of endometriosis.

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Condition tags

endometriosisinfertility

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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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