ArticleAging and disease2024
Aberrantly High FBXO31 Impairs Oocyte Quality in Premature Ovarian Insufficiency.
Article in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Differentially expressed genes and therapeutic targets for nonalcoholic fatty liver disease from transcriptomic techniques.Medicine · 2025Article
- GPD1L-Mediated Glycerophospholipid Metabolism Dysfunction in Women With Diminished Ovarian Reserve: Insights From Pseudotargeted Metabolomic Analysis of Follicular Fluid.Cell proliferation · 2025Article
- Non-coding RNA-mediated granulosa cell dysfunction during ovarian aging: From mechanisms to potential interventions.Non-coding RNA research · 2025Review
- The Intrabody Against Murine Double Minute 2 via a p53-Dependent Pathway Induces Apoptosis of Cancer Cell.International journal of molecular sciences · 2025Article
- Targeting programmed cell death with natural products: a potential therapeutic strategy for diminished ovarian reserve and fertility preservation.Frontiers in pharmacology · 2025Review
- Trajectory of primordial follicle depletion is accelerated in obese mice in response to 7,12-dimethylbenz[a]anthracene exposure†.Biology of reproduction · 2024Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Premature ovarian insufficiency (POI), which is defined as loss of ovarian function that occurs before the age of 40, causes menstrual disturbances, infertility, and diverse health problems in females. Despite the limited understanding of the molecular basis underlying POI pathology, we had previously demonstrated that the cooperation of miR-106a and FBXO31 plays a pivotal role in diminished ovarian reserve (DOR), with FBXO31 serving as a putative target of miR-106a. In this study, we found that FBXO31 is aberrantly expressed in granulosa cells of POI patients, leading to accumulated reactive oxygen species (ROS) and cell apoptosis via the p53/ROS pathway. Furthermore, our results demonstrated that high levels of FBXO31 in mouse ovaries impair oocyte quality. Our study revealed that FBXO31 may serve as a novel indicator and play a significant role in the etiology of POI.
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Registered trials
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