ArticleJournal of assisted reproduction and genetics2023
BNIP3-mediated autophagy via the mTOR/ULK1 pathway induces primordial follicle loss after ovarian tissue transplantation.
Article in Journal of assisted reproduction and genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Arfgef3 knockout ameliorates ischemia reperfusion-induced acute kidney injury via mitochondrial dysfunction alleviation in mice.Renal failure · 2025Article
- PPA1 promotes oxidative phosphorylation and malignant progression of colorectal cancer under glucose restriction via AMPK/ULK1/FUNDC1-mediated mitophagy.Cell death discovery · 2025Article
- The impact of hypoxia on the cellular phenotype and proteome of KGN cells.Reproduction & fertility · 2025Article
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
- Developing Mouse Models for Ovarian Tissue Transplantation and Xenotransplantation: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- AAA237, an SKP2 inhibitor, suppresses glioblastoma by inducing BNIP3-dependent autophagy through the mTOR pathway.Cancer cell international · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo explore the underlying mechanism of primordial follicle loss in the early period following ovarian tissue transplantation (OTT).
methodsBNIP3 was selected through bioinformatic protocols, as the hub gene related to autophagy during OTT. BNIP3 and autophagy in mice ovarian grafts and in hypoxia-mimicking KGN cells were detected using immunohistochemistry, transmission electron microscopy (TEM), western blotting, qPCR, and fluorescence staining. The regulatory role played by BNIP3 overexpression and the silencing of KGN cells in autophagy via the mTOR/ULK1 pathway was investigated.
resultsUltrastructure examination showed that autophagic vacuoles increased after mice ovarian auto-transplantation. The BNIP3 and autophagy-related proteins (Beclin-1, LC3B, and SQSTM1/p62) in mice ovarian granulosa cells of primordial follicle from ovarian grafts were altered compared with the control. Administration of an autophagy inhibitor in mice decreased the depletion of primordial follicles. In vitro experiments indicated that BNIP3 and autophagy activity were upregulated in KGN cells treated with cobalt chloride (CoCl
conclusionsBNIP3-induced autophagy is crucial in primordial follicle loss during OTT procedure, and BNIP3 is a potential therapeutic target for primordial follicle loss after OTT.
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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.