Autophagy-dependent ferroptosis is involved in the development of endometriosis

Hui Li; Huadi Yang; Shenyi Lu; Xinyan Wang; Xinhe Shi; Peiyu Mao

doi:10.1080/09513590.2023.2242962

Autophagy-dependent ferroptosis is involved in the development of endometriosis

Hui Li, Huadi Yang, Shenyi Lu, Xinyan Wang, Xinhe Shi, Peiyu Mao

Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2023 · vol. 39(1) , pp. 2242962 · doi:10.1080/09513590.2023.2242962 · PMID:37553011 · W4385649077

article OA: diamond CC0 ⤵ 11 in-corpus citations

📄 Open PDF View on OpenAlex View on PubMed View at publisher

⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Endometriosis progression is associated with autophagy-dependent ferroptosis, as evidenced by altered protein expression and experimental induction/inhibition of these processes.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

OBJECTIVE: Endometriosis (EMS) is an estrogen-dependent condition with unclear pathogenesis. Recent findings suggest implicate autophagy and ferroptosis in EMS development. METHODS: We assessed autophagy and ferroptosis proteins in EMS patients using immunohistochemistry and western blot and established an EMS rat model through allograft endometrial transplantation, confirmed via hematoxylin and eosin staining and epithelial-mesenchymal transition -related proteins. Primary EMS cells were isolated from the model rats and cultured under five conditions: control, EMS, EMS with Rapamycin (autophagy inducer), EMS with si-Atg5 (autophagy inhibitor), and EMS with si-Atg5 plus Erastin (ferroptosis inducer). We evaluated cell viability, iron content, oxidative stress, and mitochondrial morphologyin EMS cells, and detected autophagy and ferroptosis proteins through immunofluorescence, western blot, and monodansylcadaverine staining. RESULTS: Autophagy proteins Beclin1 and LC3 were highly expressed, whereas p62, glutathione peroxidase 4, and p53 were lowly expressed in EMS patients. Rapamycin decreased cell viability but increased iron content, reactive oxygen species, lipid peroxide production, the number of ferroptotic mitochondria, and the expression of autophagy proteins in EMS cells, while si-Atg5 showed opposite effects. Additionally, Erastin reversed the impact of si-Atg5 on EMS cells. CONCLUSION: Our findings suggest that autophagy-dependent ferroptosis plays a role in EMS progression.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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 (40)

Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis† via openalex
Autophagy in endometriosis. via openalex
Autophagy in endometriosis: Friend or foe? via openalex
Differences in autophagy-associated mRNAs in peritoneal fluid of patients with endometriosis and gynecologic cancers via openalex
Differential induction of autophagy by mTOR is associated with abnormal apoptosis in ovarian endometriotic cysts via openalex
Effect of matrix metalloproteinase promoter polymorphisms on endometriosis and adenomyosis risk: evidence from a meta-analysis via openalex
Endometriosis: The Role of Iron Overload and Ferroptosis via openalex
EPHA3 enhances macrophage autophagy and apoptosis by disrupting the mTOR signaling pathway in mice with endometriosis via openalex
Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology via openalex
Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis via openalex
Hypoxia-inducible factor-1α promotes endometrial stromal cells migration and invasion by upregulating autophagy in endometriosis via openalex
Increased expression of YAP is associated with decreased cell autophagy in the eutopic endometrial stromal cells of endometriosis via openalex
Iron-overloaded follicular fluid increases the risk of endometriosis-related infertility by triggering granulosa cell ferroptosis and oocyte dysmaturity via openalex
Iron overload in endometriosis peritoneal fluid induces early embryo ferroptosis mediated by HMOX1 via openalex
Iron overload–modulated nuclear factor kappa-B activation in human endometrial stromal cells as a mechanism postulated in endometriosis pathogenesis via openalex
Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis via openalex
SCM-198 Prevents Endometriosis by Reversing Low Autophagy of Endometrial Stromal Cell via Balancing ERα and PR Signals via openalex
Silencing of lncRNA MALAT1 facilitates erastin-induced ferroptosis in endometriosis through miR-145-5p/MUC1 signaling via openalex
The Methyl Ester of 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid Reduces Endometrial Lesions Development by Modulating the NFkB and Nrf2 Pathways via openalex
doi:10.1186/s13046-017-0644-8 via openalex
doi:10.1016/j.semcancer.2019.03.002 via openalex
doi:10.3390/ijms22105074 via openalex
doi:10.1371/journal.pone.0166059 via openalex
doi:10.18632/oncotarget.20771 via openalex
doi:10.3892/ijo.2015.3191 via openalex
doi:10.3390/ijms231810902 via openalex
doi:10.1016/j.cell.2017.09.021 via openalex
doi:10.1007/s00018-019-03122-4 via openalex
doi:10.1186/s12943-020-1138-4 via openalex
doi:10.1093/humupd/dmt053 via openalex
doi:10.18632/oncotarget.13890 via openalex
doi:10.18632/oncotarget.18041 via openalex
doi:10.1016/j.cell.2012.03.042 via openalex
doi:10.1038/nature13148 via openalex
doi:10.1038/s41423-021-00675-y via openalex
doi:10.1146/annurev-cellbio-120219-035530 via openalex
doi:10.3892/or.2017.6123 via openalex
W6768061876 via openalex
doi:10.1016/j.cub.2018.05.094 via openalex
doi:10.1016/j.ccell.2019.04.002 via openalex

Cited by (11)

Source provenance

europepmc: last seen: 2026-06-11T06:19:48.454388+00:00
openalex: last seen: 2026-05-10T10:52:23.898729+00:00
pubmed: last seen: 2026-05-25T00:33:36.794880+00:00

License: CC0 · commercial use OK

[1] Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis† via openalex

[2] Autophagy in endometriosis. via openalex

[3] Autophagy in endometriosis: Friend or foe? via openalex

[4] Differences in autophagy-associated mRNAs in peritoneal fluid of patients with endometriosis and gynecologic cancers via openalex

[5] Differential induction of autophagy by mTOR is associated with abnormal apoptosis in ovarian endometriotic cysts via openalex

[6] Effect of matrix metalloproteinase promoter polymorphisms on endometriosis and adenomyosis risk: evidence from a meta-analysis via openalex

[7] Endometriosis: The Role of Iron Overload and Ferroptosis via openalex

[8] EPHA3 enhances macrophage autophagy and apoptosis by disrupting the mTOR signaling pathway in mice with endometriosis via openalex

[9] Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology via openalex

[10] Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis via openalex

[11] Hypoxia-inducible factor-1α promotes endometrial stromal cells migration and invasion by upregulating autophagy in endometriosis via openalex

[12] Increased expression of YAP is associated with decreased cell autophagy in the eutopic endometrial stromal cells of endometriosis via openalex

[13] Iron-overloaded follicular fluid increases the risk of endometriosis-related infertility by triggering granulosa cell ferroptosis and oocyte dysmaturity via openalex

[14] Iron overload in endometriosis peritoneal fluid induces early embryo ferroptosis mediated by HMOX1 via openalex

[15] Iron overload–modulated nuclear factor kappa-B activation in human endometrial stromal cells as a mechanism postulated in endometriosis pathogenesis via openalex

[16] Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis via openalex

[17] SCM-198 Prevents Endometriosis by Reversing Low Autophagy of Endometrial Stromal Cell via Balancing ERα and PR Signals via openalex

[18] Silencing of lncRNA MALAT1 facilitates erastin-induced ferroptosis in endometriosis through miR-145-5p/MUC1 signaling via openalex

[19] The Methyl Ester of 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid Reduces Endometrial Lesions Development by Modulating the NFkB and Nrf2 Pathways via openalex

[20] doi:10.1186/s13046-017-0644-8 via openalex

[21] doi:10.1016/j.semcancer.2019.03.002 via openalex

[22] doi:10.3390/ijms22105074 via openalex

[23] doi:10.1371/journal.pone.0166059 via openalex

[24] doi:10.18632/oncotarget.20771 via openalex

[25] doi:10.3892/ijo.2015.3191 via openalex

[26] doi:10.3390/ijms231810902 via openalex

[27] doi:10.1016/j.cell.2017.09.021 via openalex

[28] doi:10.1007/s00018-019-03122-4 via openalex

[29] doi:10.1186/s12943-020-1138-4 via openalex

[30] doi:10.1093/humupd/dmt053 via openalex

[31] doi:10.18632/oncotarget.13890 via openalex

[32] doi:10.18632/oncotarget.18041 via openalex

[33] doi:10.1016/j.cell.2012.03.042 via openalex

[34] doi:10.1038/nature13148 via openalex

[35] doi:10.1038/s41423-021-00675-y via openalex

[36] doi:10.1146/annurev-cellbio-120219-035530 via openalex

[37] doi:10.3892/or.2017.6123 via openalex

[38] W6768061876 via openalex

[39] doi:10.1016/j.cub.2018.05.094 via openalex

[40] doi:10.1016/j.ccell.2019.04.002 via openalex