ArticleCells2022
Low WIP1 Expression Accelerates Ovarian Aging by Promoting Follicular Atresia and Primordial Follicle Activation.
Article in Cells, 2022. 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, 10 citations in OpenAlex.
- Heterogeneity in secondary follicle development buffers the lifespan of activated oocytes to optimize female fertility in mice.Nature aging · 2026Article
- Research progress on multi-mechanism analysis and protection strategies of ovarian aging and fertility decline.Journal of ovarian research · 2026Review
- Integrated analysis of differential m6A methylation and transcriptome profiles in ovaries of young and aged Qira black sheep.BMC genomics · 2026Article
- Research Hotspots and Emerging Frontiers in Ovarian Aging: A Bibliometric Analysis (2006-2025).Endocrine, metabolic & immune disorders drug targets · 2026Review
- Bulk RNA-seq conjoined with ScRNA-seq analysis reveals the molecular characteristics of nucleus pulposus cell ferroptosis in rat aging intervertebral discs.Arthritis research & therapy · 2025Article
- Extracellular vesicles in reproductive medicine: from "animal-led" to "plant-enabled".Frontiers in cell and developmental biology · 2025Review
- Sestrin1, 2, and 3 are dispensable for female fertility in mice.Journal of ovarian research · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Our previous study demonstrated that ovarian wild-type P53-induced phosphatase 1 (WIP1) expression decreased with age. We hypothesized that WIP1 activity was related to ovarian aging. The role of WIP1 in regulating ovarian aging and its mechanisms remain to be elucidated. Adult female mice with or without WIP1 inhibitor (GSK2830371) treatment were divided into three groups (Veh, GSK-7.5, GSK-15) to evaluate the effect of WIP1 on ovarian endocrine and reproductive function and the ovarian reserve. In vitro follicle culture and primary granulosa cell culture were applied to explore the mechanisms of WIP1 in regulating follicular development. This study revealed that WIP1 expression in atretic follicle granulosa cells is significantly lower than that in healthy follicles. Inhibiting WIP1 phosphatase activity in mice induced irregular estrous cycles, caused fertility declines, and decreased the ovarian reserve through triggering excessive follicular atresia and primordial follicle activation. Primordial follicle depletion was accelerated via PI3K-AKT-rpS6 signaling pathway activation. In vitro follicle culture experiments revealed that inhibiting WIP1 activity impaired follicular development and oocyte quality. In vitro granulosa cell experiments further indicated that downregulating WIP1 expression promoted granulosa cell death via WIP1-p53-BAX signaling pathway-mediated apoptosis. These findings suggest that appropriate WIP1 expression is essential for healthy follicular development, and decreased WIP1 expression accelerates ovarian aging by promoting follicular atresia and primordial follicle activation.
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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.