ArticleInternational journal of molecular sciences2016
Follicle Loss and Apoptosis in Cyclophosphamide-Treated Mice: What's the Matter?
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Comparative Meta-analysis of Adipose Tissue Transcriptomics Data in PCOS Patients and Healthy Control Women.Reproductive sciences (Thousand Oaks, Calif.) · 2023Pooled it
- From Maternal Exposure to F1 Development: Unveiling Cyclophosphamide-Induced Reproductive Toxicity.Biomedicines · 2026Article
- Surgical approaches to fertility preservation in the cancer patient: current and future directions.Frontiers in endocrinology · 2026Review
- Carvacrol ameliorates cyclophosphamide-induced rat premature ovarian failure and uterine fibrosis via regulating PI3K/AKT/FOXO3a signaling pathway.Journal of ovarian research · 2025Article
- The role of mammalian target of rapamycin inhibitors in mitigating cyclophosphamide-induced ovarian damage in a murine model.Clinical and experimental reproductive medicine · 2025Article
- Bioengineered ovary reconstructs follicle-like structures in a mouse model of chemotherapy-induced premature ovarian failure.Stem cell research & therapy · 2025Article
- Melatonin alleviates cyclophosphamide-induced ovarian toxicity in mice.Journal of assisted reproduction and genetics · 2025Article
- Nano-curcumin potentially ameliorates hormonal function and follicular counts following the vitrification and transplantation of rat ovarian tissue.Scientific reports · 2025Article
- Nicotinamide mononucleotide protects ovarian function and oocyte developmental competence during chemotherapy.Journal of ovarian research · 2025Article
- Fertility Protection in Female Cancer Patients: From Molecular Mechanisms of Gonadotoxic Therapies to Pharmacotherapeutic Possibilities.International journal of molecular sciences · 2025Review
- Does gonadotoxic chemotherapy deplete the ovarian reserve through activation of primordial follicles?Human reproduction (Oxford, England) · 2025Article
- BCAA metabolism: the Achilles' heel of ovarian cancer, polycystic ovary syndrome, and premature ovarian failure.Frontiers in endocrinology · 2025Review
- Regulation of follicular activation signaling pathways by in vitro inhibition of YAP/TAZ activity in mouse ovaries.Scientific reports · 2023Article
- Amniotic fluid-derived exosomes attenuated fibrotic changes in POI rats through modulation of the TGF-β/Smads signaling pathway.Journal of ovarian research · 2023Article
- Tamoxifen decreases ovarian toxicity without compromising cancer treatment in a rat model of mammary cancer.BMC genomics · 2023Article
- Lyophilized equine platelet-rich plasma (L-GFJournal of ovarian research · 2023Article
- An evaluation of the effects on the ovaries of hyperbaric oxygen therapy in a rat model of premature ovarian failure created with cyclophosphamide.Turkish journal of obstetrics and gynecology · 2023Article
- VX-765 has a Protective Effect on Mice with Ovarian Injury Caused by Chemotherapy.Current cancer drug targets · 2023Article
- DNA Damage Stress Response and Follicle Activation: Signaling Routes of Mammalian Ovarian Reserve.International journal of molecular sciences · 2022Review
- Classical music restored fertility status in rat model of premature ovarian failure.BMC complementary medicine and therapies · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With increasing numbers of young female cancer survivors following chemotherapy, chemotherapy-induced fertility loss must be considered. Menstrual disorder and infertility are of particular concern in female cancer patients. We showed that treatment with the alkylating agent cyclophosphamide (CTX) could cause severe primordial follicle loss and growing follicle apoptosis, resulting in loss of ovarian reserve. SPF C57BL/6 female mice were treated with a single dose of 120 mg/kg of CTX or saline as a control, and both sides of ovaries were collected three or seven days after injection. Following CTX treatment, the ovaries were mostly composed of collapsed oocytes and presented marked cortical fibrosis and a reduced number of follicles, especially primordial follicles. The loss of primordial follicles was confirmed by primordial follicle counting, immunohistochemistry and Western blot detection of DDx4/MVH. Follicle apoptosis was tested by a TUNEL assay and the number of TUNEL-positive follicle cells increased, as expected, in CTX-treated mice. Furthermore, expression of APAF-1 and cleaved caspase-3 was also increased after CTX treatment. Analysis of the PI3K/Akt/mTOR signaling pathway showed that CTX increased phosphorylation of Akt, mTOR and downstream proteins without affecting total levels. These results demonstrated that the CTX treatment led to the hyperactivation of the PI3K/Akt/mTOR signaling pathway in ovaries which may be related to primordial follicle loss and growing follicle apoptosis.
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