Chemotherapy-Induced Ovarian Toxicity and Fertility Preservation
Summary
Chemotherapy-induced ovarian toxicity constitutes a major iatrogenic challenge in the management of premenopausal women with cancer. Alkylating agents, platinum compounds and anthracyclines can inflict direct DNA damage to oocytes and granulosa cells, provoking apoptosis, aberrant activation of dormant follicles and stromal fibrosis. The resultant depletion of the primordial follicle pool leads to diminished ovarian reserve, impaired endocrine function and heightened risk of premature ovarian insufficiency. Beyond cell-autonomous effects, chemotherapy perturbs the ovarian microenvironment by inducing oxidative stress, vascular compromise and inflammatory remodelling, further compromising follicular survival and quality.
The urgent clinical imperative to preserve fertility has driven the development of multiple strategies. Pharmacological adjuvants aim to inhibit DNA damage signalling or to scavenge reactive oxygen species. Cryopreservation of oocytes, embryos or ovarian tissue remains the only established route to safeguard reproductive potential, while emerging regenerative approaches seek to restore ovarian function in situ.
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Chemotherapy-Induced Ovarian Toxicity and Fertility Preservation publication trend
The graph below shows the total number of articles in chemotherapy-induced ovarian toxicity and fertility preservation across all publications each year (not limited to Nature Index journals).
Technical terms
Primordial follicle: a resting oocyte surrounded by pregranulosa cells representing the non-renewable ovarian reserve.
Ovarian reserve: the total population of primordial and growing follicles capable of sustaining fertility and hormone production.
Oxidative stress: an imbalance between reactive oxygen species and antioxidant defences leading to cellular damage.
Ferroptosis: a form of programmed cell death driven by iron-dependent lipid peroxidation and mitochondrial dysfunction.
Granulosa cells: somatic cells that support oocyte maturation and secrete sex steroids within the follicle.
Mesenchymal stem cells: multipotent stromal cells with regenerative potential, capable of homing to injured ovarian tissue.
References
- Ovarian microenvironment: challenges and opportunities in protecting against chemotherapy-associated ovarian damage. Human Reproduction Update (2024).
- Chemotherapy impairs ovarian function through excessive ROS-induced ferroptosis. Cell Death & Disease (2023).
- Pyrroloquinoline quinone promotes human mesenchymal stem cell-derived mitochondria to improve premature ovarian insufficiency in mice through the SIRT1/ATM/p53 pathway. Stem Cell Research & Therapy (2024).
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