ArticleJournal of ovarian research2025
Granulosa cell-specific FOXJ2 overexpression induces premature ovarian insufficiency by triggering apoptosis via mitochondrial calcium overload.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Lysine-specific demethylase 3A (KDM3A) protects against ovarian dysfunction in premature ovarian insufficiency by transcriptional activation of ATP-binding cassette sub-family A member 7 (ABCA7)-mediated mitochondrial homeostasis.Molecular biomedicine · 2026Article
- Maternal hyperhomocysteinemia compromises female offspring fertility through overactivation of primordial follicles.iScience · 2026Article
- Mechanisms of mitochondrial dysfunction in premature ovarian insufficiency.Journal of ovarian research · 2026Review
- Targeting MFF succinylation: a novel therapeutic strategy for premature ovarian insufficiency by restoring mitochondrial dynamics in granulosa cells.Journal of ovarian research · 2026Review
- Mitochondrial CaFrontiers in cell and developmental biology · 2026Review
- Inflammatory remodeling of the ovarian microenvironment in premature ovarian insufficiency: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Metabolomic Analysis Identifies Betaine as a Key Mediator ofInternational journal of molecular sciences · 2025Article
- Transcriptome Sequencing Reveals the Molecular Mechanism of Heat Stroke-Induced Myocardial Injury.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundFollicle development is a complicated biological process that produces mature oocytes, and requires nutrients, growth factors, and steroids produced by ovarian granulosa cells (GCs). High fork head box J2 (FOXJ2) expression might negatively regulate ovarian function; however, the mechanism is unclear. This study aimed to investigate the effect and mechanism of FOXJ2 overexpression in GCs on regulating follicle development and fertility.
methodsA GC-specific conditional Foxj2 knock-in mouse model (Amh-cre; Foxj2
resultsFOXJ2 overexpression in GCs led to reduced fertility, hormonal abnormalities, and follicle atresia, starting at the initiation of sexual maturity, resulting in a premature ovarian insufficiency (POI)-like phenotype. Increased apoptosis and mitochondrial calcium overload were detected in the GCs of Amh-cre; Foxj2
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