ArticleJournal of ovarian research2017
Rapamycin Prevents cyclophosphamide-induced Over-activation of Primordial Follicle pool through PI3K/Akt/mTOR Signaling Pathway in vivo.
Article in Journal of ovarian research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 137 citations in OpenAlex.
- Research progress on multi-mechanism analysis and protection strategies of ovarian aging and fertility decline.Journal of ovarian research · 2026Review
- Novel anti-Mullerian hormone receptor 2 binding peptide prevents chemotherapy-related ovarian follicle loss in a mouse model.Journal of assisted reproduction and genetics · 2026Article
- The role of anti-Müllerian hormone as a therapeutic agent to preserve the ovarian follicle pool during chemotherapy.Journal of assisted reproduction and genetics · 2026Review
- Article
- Therapeutic Effects of Stromal Stem Cells Derived from Ovarian Tissue in a Cyclophosphamide-Induced Rat Model of Ovarian Failure.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Drug-induced gastrointestinal toxicity and barrier integrity: cytoskeleton-mediated impairment in a clinically relevant human intestinal epithelium model.Experimental & molecular medicine · 2026Article
- Female fertility preservation: 25 years of progress, expanding indications and future prospects.Human reproduction update · 2026Review
- DNA damage response signaling in oocytes from an oncofertility perspective†.Biology of reproduction · 2026Review
- Pyroptosis in premature ovarian insufficiency: pathogenic mechanisms, pathway crosstalk, and therapeutic strategies.Frontiers in medicine · 2026Review
- Combination olaparib and cyclophosphamide cancer therapy exacerbates ovarian reserve depletion in mice with conditional loss ofFrontiers in endocrinology · 2026Article
- Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The Effect of AMH on Folliculogenesis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Selenium nanoparticles mitigate Cyclophosphamide-Induced premature ovarian failures in mice by activating PI3K/AKT signaling pathway and inhibiting ferroptosis.Journal of ovarian research · 2025Article
- Metabolomic Analysis of Sea Cucumber Ovum Hydrolysates in Cyclophosphamide-Induced Premature Ovarian Failure.Foods (Basel, Switzerland) · 2025Article
- Integrated analysis of microRNA and mRNA interactions regulating fecundity in the ovaries of two distinct sheep breeds.BMC genomics · 2025Article
- Premature ovarian insufficiency restoration after chemotherapy: current achievements and future prospects on its treatment or management.Journal of ovarian research · 2025Review
- Exogenous melatonin alleviates premature ovarian failure by regulating granulosa cell autophagy.NPJ Regenerative medicine · 2025Article
- The potential of low-intensity pulsed ultrasound to apply the long-term ovary protection from injury induced by 4-vinylcyclohexene diepoxide through inhibiting granulosa cell apoptosis.Bioengineering & translational medicine · 2025Article
- Does gonadotoxic chemotherapy deplete the ovarian reserve through activation of primordial follicles?Human reproduction (Oxford, England) · 2025Article
- Intrinsic differences in mTOR activity mediates lineage-specific responses to cyclophosphamide in mouse and human granulosa cells.Journal of ovarian research · 2025Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrimordial follicular depletion has thought to be a common adverse effect of chemotherapy especially for female of reproductive age. The study aimed to evaluate the protective effect of rapamycin on the primordial follicles and its potential mechanism for patients receiving chemotherapy.
methods8-week old BALB/c female mice were randomly assigned into four groups (control; rapamycin; cyclophosphamide; and rapamycin combined with cyclophosphamide). Hematoxylin staining, immunohistochemical, TUNEL, western blotting and ELISA were employed to assess inter-group differences using Student's t-test and Mann-Whitney test.
resultsCyclophosphamide depleted the follicular reserve and induced the phosphorylation of the key proteins of PI3K/Akt/mTOR pathway in mice in a dose-dependent manner. Co-treatment with rapamycin significantly reduced primordial follicle loss at all cyclophosphamide dose groups and prevent the follicle growth wave caused by cyclophosphamide treatment (P < 0.05). TUNEL staining showed that no apoptosis occured in the primordial follicles in all groups and fewer apoptosis in large growing follicles were observed in ovaries from rapamycin + cyclophosphamide group compared to that received cyclophosphamide alone. Serum anti-Müllerian hormone (AMH) was significantly reduced in cyclophosphamide alone group, in contrast to the normal level in rapamycin + cyclophosphamide group. Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P < 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.
conclusionsRapamycin can prevent the primordial follicle activation induced by cyclophosphamide through PI3K/Akt/mTOR signaling pathway and thus plays a role in preserving the follicle pool. These results suggest that rapamycin may be an effective protection for ovarian function during chemotherapy, which means a new nonsurgical application for protection of ovarian reserve and prevention of POF.
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