ArticleInternational journal of molecular sciences2021
Autophagy and Mitophagy Promotion in a Rat Model of Endometriosis.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- WERF Endometriosis Phenome and Biobanking Harmonisation Project for Experimental Models in Endometriosis Research (EPHect-EM-Homologous): homologous rodent models.Molecular human reproduction · 2025Pooled it
- Molecular Insights Into Endometriosis for Early Detection and Therapeutic Targets.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- NET-DNA Activates the ANXA2/TMEM215/BiP Axis to Promote Mitophagy-Mediated Anoikis Resistance in Endometriosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities.iScience · 2026Review
- SIRT1-mediated deacetylation of HMGB1 promotes the progression of endometriosis by regulating autophagy.Scientific reports · 2026Article
- Consumption of Cashew Nuts on Oxidative Stress and Neuroinflammation Markers in Methionine-Induced Hyperhomocysteinemia in Rats.Food science & nutrition · 2026Article
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
- Natural products modulate programmed cell death signaling mechanism for treating endometriosis: a review.Frontiers in pharmacology · 2026Review
- Parthenolide attenuated the endometriosis-like lesions by activating autophagy and suppressing NLRP3 inflammasome activity.Iranian journal of basic medical sciences · 2026Article
- Dysregulated autophagy in endometriosis: molecular mechanisms, controversies, and clinical implications.Reproductive biology and endocrinology : RB&E · 2025Review
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Unveiling the vital role of OGG1 in inflammation, vascular endothelial damage, and cell death in obstetric and gynecological diseases.Human cell · 2025Review
- Erastin-induced multi-pathway cell death in endometriosis: a mechanistic and translational narrative review.Frontiers in medicine · 2025Review
- The role of mitophagy in female reproductive system diseases: from molecular mechanisms to therapeutic strategies.Frontiers in endocrinology · 2025Review
- Molecular mechanisms and Biological Functions of Autophagy in Endometrial Diseases.International journal of medical sciences · 2025Review
- New insights on mitochondrial heteroplasmy observed in ovarian diseases.Journal of advanced research · 2024Review
- Focusing on the role of protein kinase mTOR in endometrial physiology and pathology: insights for therapeutic interventions.Molecular biology reports · 2024Review
- Causal relationship between antihypertensive drugs and Hashimoto's thyroiditis: a drug-target Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Prohibitin2/PHB2, Transcriptionally Regulated by GABPA, Inhibits Cell Growth via PRKN/Parkin-dependent Mitophagy in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- The constructive and destructive impact of autophagy on both genders' reproducibility, a comprehensive review.Autophagy · 2023Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis is a gynecological condition affecting patients in reproductive age. The aim of this paper was to assess the effects of the autophagy and mitophagy induction in a rat model of endometriosis. Endometriosis was induced by the injection of uterine fragments, and rapamycin (0. 5 mg/kg) was administered once per week. One week from the induction, rats were sacrificed, and laparotomy was performed to collect the endometriotic implants and to further process them for molecular analysis. Western blot analysis was conducted on explanted lesions to evaluate the autophagy pathway during the pathology. Elevated phospho-serine/threonine kinase (p-AKT) and mammalian target of rapamycin (mTOR) expressions were detected in vehicle-treated rats, while Beclin and microtubule-associated protein 1A/1B-light chain 3 II (LC3II) expressions were low. Additionally, samples collected from vehicle groups indicated low Bnip3, Ambra1, and Parkin expressions, demonstrating impaired autophagy and mitophagy. Rapamycin administration reduced p-AKT and mTOR expressions and increased Beclin and LC3II, Bnip3, Ambra1, and Parkin expressions, activating both mechanisms. We also evaluated the impact of the impaired autophagy and mitophagy pathways on apoptosis and angiogenesis. Rapamycin was administered by activating autophagy and mitophagy, which increased apoptosis (assessed by Western blot analysis of Bcl-2, Bax, and Cleaved-caspase 3) and reduced angiogenesis (assessed by immunohistochemical analysis of vascular endothelial grow factor (VEGF) and CD34) in the lesions. All of these mechanisms activated by the induction of the autophagy and mitophagy pathways led to the reduction in the lesions' volume, area and diameter.
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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.