ArticleJournal of ovarian research2024
Cyclophosphamide induces ovarian granulosa cell ferroptosis via a mechanism associated with HO-1 and ROS-mediated mitochondrial dysfunction.
Article in Journal of ovarian research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The interaction between endoplasmic reticulum stress and ferroptosis in ovarian diseases.Journal of ovarian research · 2026Pooled it
- Mitochondria as integrative regulators of ferroptosis in the female reproductive system.Biology of reproduction · 2026Review
- Central nervous system resilience to cyclophosphamide: preserved behavior, astrocytes and LGALS3 expression in immunosuppressed mice.Brain, behavior, & immunity - health · 2026Article
- Spatial Transcriptomic Atlas Reveals That Forkhead Box O3-Mediated Mitochondrial Dynamics Imbalance Drives Premature Ovarian Insufficiency in Mice.Aging cell · 2026Article
- Technological Advances of Cryopreservation in Ovarian Tissue for Female Children: Exploring the Molecular Insights and Mechanisms.International journal of molecular sciences · 2026Review
- Yam Protects Immunocompromised Mice from Influenza Infection via the Gut-SCFA-GPCR-Immune Axis.Nutrients · 2026Article
- Age-related GSS promoter methylation in BMSCs drives osteoporosis and the reversal by targeted GSH delivery.Bioactive materials · 2026Article
- Primed Avian Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Restore Granulosa Cell Homeostasis in a CTX-Induced POI-like Dysfunction Model Under Human Menopausal Gonadotropin Stimulation.International journal of molecular sciences · 2026Article
- Urolithin A-Enhanced Multi-Bioactive Formulation Mitigates Cyclophosphamide-Induced Premature Ovarian Failure Through Suppression of Oxidative-Inflammatory Stress and Preservation of Follicle Fate.Antioxidants (Basel, Switzerland) · 2026Article
- Immediate protective effect of rUCMSC-EVs on ovarian function in a cyclophosphamide -induced premature ovarian insufficiency rats: counteracting granulosa cell apoptosis.Journal of ovarian research · 2026Article
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
- Research Progress on Ferroptosis Regulation of Female Reproduction.Biological trace element research · 2026Review
- HuMSCs-derived exosomes alleviate premature ovarian insufficiency by enhancing SIRT3-mediated mitochondrial function in theca-interstitial cells.Journal of ovarian research · 2026Article
- Engineered Cas9 exosome vesicles as a novel gene editing tool for targeted ASPN editing in osteoarthritis.Journal of nanobiotechnology · 2026Article
- Mesenchymal stem cell therapy for premature ovarian insufficiency: progress and challenges.Journal of ovarian research · 2026Review
- Hydrogen treatment attenuates ferroptosis and alleviates spinal cord ischemia-reperfusion injury by activating the Nrf2/HO-1 signaling pathway.Molecular biology reports · 2026Article
- Oxidative Stress andInternational journal of molecular sciences · 2026Review
- HucMSC-derived exosomes alleviate chemotherapy-induced premature ovarian insufficiency via SMURF1-mediated inhibition of ferroptosis in ovarian granulosa cells.Stem cell research & therapy · 2026Article
- Retinoic Acid and Calcitriol Protect Mouse Primordial Follicles from Cyclophosphamide Treatment-Induced Apoptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Article
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Abstract
Abnormal granulosa cell (GC) death contributes to cyclophosphamide (CTX) induced primary ovarian insufficiency (POI). To investigate the contribution of GCs to POI, gene profiles of GCs exposed to CTX were assessed using RNA-Seq and bioinformatics analysis. The results showed the differentially expressed genes (DEGs) were enriched in the ferroptosis-related pathway, which is correlated with upregulated heme oxygenase 1 (HO-1) and downregulated glutathione peroxidase-4 (GPX4). Using CTX-induced cell culture (COV434 and KGN cells), the levels of iron, reactive oxygen species (ROS), lipid peroxide, mitochondrial superoxide, mitochondrial morphology and mitochondrial membrane potential (MMP) were detected by DCFDA, MitoSOX, C11-BODIPY, MitoTracker, Nonylacridine Orange (NAO), JC-1 and transmission electron microscopy respectively. The results showed iron overload and disrupted ROS, including cytoROS, mtROS and lipROS homeostasis, were associated with upregulation of HO-1 and could induce ferroptosis via mitochondrial dysfunction in CTX-induced GCs. Moreover, HO-1 inhibition could suppress ferroptosis induced GPX4 depletion. This implies a role for ROS in CTX-induced ferroptosis and highlights the effect of HO-1 modulators in improving CTX-induced ovarian damage, which may provide a theoretical basis for preventing or restoring GC and ovarian function in patients with POI.
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