FDX1 enhances endometriosis cell cuproptosis via G6PD-mediated redox homeostasis

Jiayi Lu, Xi Ling, Yonghong Sun, Lu Liu, Lan Liu, Xiaoyun Wang, Chao Lu, Chao Lü, Chune Ren, Xue Han, Zhenhai Yu
Apoptosis : an international journal on programmed cell death · 2023 · vol. 28(7-8) , pp. 1128–1140 · doi:10.1007/s10495-023-01845-1 · PMID:37119432 · W4367368904
article OA: closed CC0 ⤵ 7 in-corpus citations
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

Ferredoxin 1 (FDX1) promotes cuproptosis in endometriosis cells by interacting with G6PD, reducing its stability and thereby lowering NADPH and GSH levels to repress cell proliferation and metastasis.

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

The paper investigates whether cuproptosis, a mitochondrial TCA cycle–associated form of programmed cell death, affects endometriosis progression, and examines the molecular regulators of this process. Using endometriosis cell models and a mouse model of ectopic endometrial tissue, the authors report that cuproptosis suppresses endometriosis cell growth and ectopic tissue growth, and that FDX1 promotes cuproptosis in endometriosis cells. Mechanistically, FDX1 interacts with G6PD to reduce its protein stability, lowering NADPH and GSH and thereby enhancing cuproptosis, which is linked to reduced proliferation and metastasis. A stated limitation/caveat is that the authors’ mechanistic conclusions derive from their experimental system(s) and that “functions of cuproptosis in endometriosis progression are still unknown” prior to their work. This paper is centrally about endometriosis — it specifically focuses on FDX1-mediated cuproptosis via a G6PD redox pathway in endometriosis cells and ectopic endometrial tissue.

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Abstract

Cuproptosis is a new form of programmed cell death, which is associated with the mitochondrial TCA (tricarboxylic acid) cycle. But the functions of cuproptosis in endometriosis progression are still unknown. Here, we find that cuproptosis suppresses the growth of endometriosis cells and the growth of ectopic endometrial tissues in a mouse model. FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which predominantly affects the cellular redox-regulating systems. Then, the reduced G6PD activity enhances cuproptosis via down-regulating NADPH and GSH levels. Collectively, our study demonstrates that FDX1 mediates cuproptosis in endometriosis via G6PD pathway, resulting in repression of endometriosis cell proliferation and metastasis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Animals

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