ArticleCell death & disease2024
Protein phosphatase 4 maintains the survival of primordial follicles by regulating autophagy in oocytes.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- From subclinical ovarian damage to reproductive outcomes: a translational perspective on PI3K/AKT/mTOR signaling in fertility preservation.Journal of assisted reproduction and genetics · 2026Review
- Brain Serotonin Deficiency Impairs Ovarian Reserve Function via the Hypothalamic-Pituitary-Ovarian Axis.Neuroscience bulletin · 2026Article
- Indole-3-carbinol alleviates cisplatin-induced ovarian damage by inhibiting ovarian fibrosis through the TGF-β1/Smad pathway.Journal of ovarian research · 2026Article
- Effect of cAMP concentration on apoptosis of sheep granulosa cells in vitro.In vitro cellular & developmental biology. Animal · 2026Article
- Autophagy in ovary: protective roles, pathological consequences, and unresolved issues.Journal of ovarian research · 2025Review
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Mechanisms of programmed cell death in livestock follicular development and atresia: a review.Journal of animal science and biotechnology · 2025Review
- Mechanisms of follicular atresia: focus on apoptosis, autophagy, and ferroptosis.Frontiers in endocrinology · 2025Review
- Non-hormone replacement therapy to overcome premature ovarian insufficiency: advances in natural products and stem cells targeting autophagy.Frontiers in endocrinology · 2025Review
- Dynamic changes in the transcriptome and metabolome of pig ovaries across developmental stages and gestation.BMC genomics · 2024Article
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Authors and funding
8 authors.
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Abstract
In mammalian ovary, the primordial follicle pool serves as the source of developing follicles and fertilizable ova. To maintain the normal length of female reproductive life, the primordial follicles must have adequate number and be kept in a quiescent state before menopause. However, the molecular mechanisms underlying primordial follicle survival are poorly understood. Here, we provide genetic evidence showing that lacking protein phosphatase 4 (PPP4) in oocytes, a member of PP2A-like subfamily, results in infertility in female mice. A large quantity of primordial follicles has been depleted around the primordial follicle pool formation phase and the ovarian reserve is exhausted at about 7 months old. Further investigation demonstrates that depletion of PPP4 causes the abnormal activation of mTOR, which suppresses autophagy in primordial follicle oocytes. The abnormal primordial follicle oocytes are eventually erased by pregranulosa cells in the manner of lysosome invading. These results show that autophagy prevents primordial follicles over loss and PPP4-mTOR pathway governs autophagy during the primordial follicle formation and dormant period.
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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 Socratic graph.