ArticleBiochemistry and biophysics reports2018
Autophagy-disrupted LC3 abundance leads to death of supporting cells of human oocytes.
Article in Biochemistry and biophysics reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.
- Beyond apoptosis: evidence of other regulated cell death pathways in the ovary throughout development and life.Human reproduction update · 2023Pooled it
- Chronic endometritis and altered embryo implantation: a unified pathophysiological theory from a literature systematic review.Journal of assisted reproduction and genetics · 2020Pooled it
- RNA splicing in cancer cell death regulation: shedding light on the molecular mechanisms and potential clinical applications.Cell death & disease · 2026Review
- Targeting Cancer Cell Fate: Apoptosis, Autophagy, and Gold Nanoparticles in Treatment Strategies.Current issues in molecular biology · 2025Review
- Article
- The role of autophagy in brain health and disease: Insights into exosome and autophagy interactions.Heliyon · 2024Review
- The constructive and destructive impact of autophagy on both genders' reproducibility, a comprehensive review.Autophagy · 2023Review
- Moschus ameliorates glutamate-induced cellular damage by regulating autophagy and apoptosis pathway.Scientific reports · 2023Article
- The Roles of Autophagy in the Genesis and Development of Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Long-Term Copper Exposure Induced Excessive Autophagy of the Porcine Spleen.Biological trace element research · 2023Article
- Trehalose Suppresses Lysosomal Anomalies in Supporting Cells of Oocytes and Maintains Female Fertility.Nutrients · 2022Article
- Autophagy in ovary and polycystic ovary syndrome: role, dispute and future perspective.Autophagy · 2021Review
- Primate-specific POTE-actin gene could play a role in human folliculogenesis by controlling the proliferation of granulosa cells.Cell death discovery · 2021Article
- Keap1 inhibition sensitizes head and neck squamous cell carcinoma cells to ionizing radiation via impaired non-homologous end joining and induced autophagy.Cell death & disease · 2020Article
- Knockdown of Atg7 Induces Nuclear-LC3 Dependent Apoptosis and Augments Chemotherapy in Colorectal Cancer Cells.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagic recycling of cell parts is generally termed as the opposite of cell death. Here, we explored the relation between cell death and autophagy by examining granulosa cell layers that control oocyte quality, which is important for the success of fertilization. Granulosa cell layers were collected from infertile women and morphologically divided into four types, viz., mature (MCCs), immature (ICCs), and dysmature cumulus cells (DCCs), and mural granulosa cells (MGCs). Microtubule-associated protein light chain 3 (LC3), which is involved in autophagosome formation, was expressed excessively in DCCs and MGCs, and their chromosomal DNA was highly fragmented. However, autophagy initiation was limited to MGCs, as indicated by the expression of membrane-bound LC3-II and autophagy-related protein 7 (ATG7), an enzyme that converts LC3-I to LC3-II. Although pro-LC3 was accumulated, autophagy was disabled in DCCs, resulting in cell death. Our results suggest the possibility that autophagy-independent accumulation of pro-LC3 proteins leads to the death of human granulosa cells surrounding the oocytes and presumably reduces oocyte quality and female fertility.
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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.