ArticlePloS one2016
Oxidative Stress Induces Mouse Follicular Granulosa Cells Apoptosis via JNK/FoxO1 Pathway.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- Iron overload in steatotic hepatocytes drives systemic metabolic dysfunction via alterations in hepatokine production.The Journal of clinical investigation · 2026Article
- Maternal Obesity Programs Adipogenic Commitment in Neonatal Mesenchymal Stem Cells: A Link to Redox-Dependent FOXO1 Signaling.Journal of cellular physiology · 2026Article
- Analysis of the resistance of small peptides from Periplaneta americana to HScientific reports · 2026Article
- BRCA1 alleviates inflammation, oxidative stress, and ovarian granulosa cell apoptosis by inhibiting endoplasmic reticulum stress, thereby ameliorating polycystic ovary syndrome.European journal of medical research · 2026Article
- A Two-Hit Hypothesis for Chemotherapy-Induced Primary Ovarian Insufficiency in Asian Populations: A Population-Specific Mechanistic Framework Linking Genetic Susceptibility and Cytotoxic Stress via the PI3K-AKT-FOXO3 Axis.BioMed research international · 2026Review
- Paeonol protects against cisplatin-induced premature ovarian failure via anti-inflammatory and antioxidant activities: an integrated approach of network pharmacology, molecular dynamics simulation, and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Molecular Regulation of FOXO1 and Its Pathophysiological Significance in Endometriosis: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- The roles of MAPK signaling pathway in ovarian folliculogenesis.Journal of ovarian research · 2025Review
- Role of Granulosa Cell Dysfunction in Women Infertility Associated with Polycystic Ovary Syndrome and Obesity.Biomolecules · 2025Review
- FoxO1 Alleviates the Mitochondrial ROS Levels Induced by α-Synuclein Preformed Fibrils in BV-2 Microglial Cells.Inflammation · 2025Article
- Bioinformatics identification of key genes and therapeutic targets for exercise intervention in polycystic ovary syndrome.Frontiers in genetics · 2025Review
- Oxidative stress and energy metabolism abnormalities in polycystic ovary syndrome: from mechanisms to therapeutic strategies.Reproductive biology and endocrinology : RB&E · 2024Review
- GNature communications · 2024Article
- The effect of Toxoplasma gondii infection on galectin-9 expression in decidual macrophages contributing to dysfunction of decidual NK cells during pregnancy.Parasites & vectors · 2024Article
- Forkhead box O proteins: steering the course of stem cell fate.Cell regeneration (London, England) · 2024Review
- Decreased HAT1 expression in granulosa cells disturbs oocyte meiosis during mouse ovarian aging.Reproductive biology and endocrinology : RB&E · 2023Article
- JNK Cascade-Induced Apoptosis-A Unique Role in GqPCR Signaling.International journal of molecular sciences · 2023Review
- Article
- FoxO1 as a tissue-specific therapeutic target for type 2 diabetes.Frontiers in endocrinology · 2023Review
- Impairment of Decidualization of Endometrial Stromal Cells by hsa-miR-375 Through NOX4 Targeting.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Jun N-terminal protein kinase (JNK) plays an important role in the regulation of cell apoptosis. Forkhead box O (FoxO) transcription factors are involved in diverse biological processes, including cellular metabolism, cell apoptosis, and cell cycle. However, the JNK/FoxO1 pathway involved in the process of apoptosis induced by oxidative stress remains to be elucidated. Here, we demonstrated that the JNK activity significantly increased in response to oxidative stress in mouse follicular granulosa cells (MGCs). SP600125, a selective JNK inhibitor, attenuated the oxidative stress-induced MGCs apoptosis. Oxidative stress enhanced the FoxO1 nuclear translocation by activating the JNK activity. Moreover, JNK mediated the dissociation of FoxO1 from 14-3-3 proteins in MGCs after the treatment with H2O2. Finally, oxidative stress up-regulated the expression of FoxO1 via JNK mediation of FoxO1 self-regulation in MGCs. Taken together, our findings suggest that JNK/FoxO1 is involved in the regulation of oxidative stress-induced cell apoptosis in MGCs.
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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.