ArticleBiology of reproduction2018
Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis.
Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- The role of the SIRT1/FOXO1 axis in regulating autophagy and inflammation in endometriosis.Journal of translational medicine · 2026Article
- Hypoxia-induced regulations of cell adhesion molecules and their implications for pathogenesis, diagnosis, and treatment of endometriosis.Frontiers in molecular biosciences · 2026Review
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
- Dysregulated autophagy in endometriosis: molecular mechanisms, controversies, and clinical implications.Reproductive biology and endocrinology : RB&E · 2025Review
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
- Expression profiles of E-cadherin and N-cadherin in endometriosis and other gynecological diseases towards targeted treatment: a systematic review.Obstetrics & gynecology science · 2025Article
- Endometriosis development in relation to hypoxia: a murine model study.Molecular medicine (Cambridge, Mass.) · 2024Article
- Effects of metformin and ganirelix on subcutaneous endometriosis in a mouse model of autophagy-related cell death.Turkish journal of obstetrics and gynecology · 2023Article
- Integrated bioinformatic analysis of dysregulated microRNA-mRNA co-expression network in ovarian endometriosis.Acta obstetricia et gynecologica Scandinavica · 2022Article
- The Role of Abnormal Uterine Junction Zone in the Occurrence and Development of Adenomyosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- Defective autophagy contributes to endometrial epithelial-mesenchymal transition in intrauterine adhesions.Autophagy · 2022Article
- CCL20/CCR6 axis mediates macrophages to promote proliferation and migration of ESCs by blocking autophagic flux in endometriosis.Stem cell research & therapy · 2022Article
- Role for autophagy-related markers Beclin-1 and LC3 in endometriosis.BMC women's health · 2022Article
- Role of GLI1 in Hypoxia-Driven Endometrial Stromal Cell Migration and Invasion in Endometriosis.Computational and mathematical methods in medicine · 2022Article
- Exploring Epithelial-Mesenchymal Transition Signals in Endometriosis Diagnosis and In Vitro Fertilization Outcomes.Biomedicines · 2021Article
- Bioinformatic analysis reveals the importance of epithelial-mesenchymal transition in the development of endometriosis.Scientific reports · 2020Article
- The Pathogenesis of Adenomyosis vis-à-vis Endometriosis.Journal of clinical medicine · 2020Review
- Article
- NLRC5 Inhibits Inflammation of Secretory Phase Ectopic Endometrial Stromal Cells by Up-Regulating Autophagy in Ovarian Endometriosis.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Endometriosis is a benign gynecologic disorder, and presents with malignant characteristics, such as migration and invasion. Hypoxia has been implicated in triggering epithelial-mesenchymal transition (EMT). Hypoxia is also known to induce autophagy. However, the relationship between autophagy and EMT under hypoxia conditions in endometriosis remains unknown. In the present study, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), microtubule associated protein light chain 3 (LC3), and mesenchymal cell marker vimentin was significantly higher in ectopic endometrium from patients with endometriosis, along with decreased expression of epithelial cell marker E-cadherin. After hypoxia treatment, endometrial epithelial cells exhibited enhanced migration and invasion abilities, as well as promoted autophagy and the EMT phenotype. Our analyses also show that HIF-1α was responsible for induction of autophagy. Moreover, inhibition of autophagy by chemical or genetic approaches suppressed hypoxia triggered EMT and reduced cell migration and invasion. Collectively, our findings identify that autophagy is critical for the migration and invasion of endometrial cells through the induction of EMT and indicate that inhibition of autophagy may be a novel useful strategy in the treatment of endometriosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.