Chemotherapy-Associated Ovarian Damage: Pathological Mechanisms and Current Interventions.
- 1The First Clinical College, Shandong University of Traditional Chinese Medicine, Jinan, People's Republic of China.
- 2Department of Gynecology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People's Republic of China.
- 3Reproductive and Genetic Center of Integrative Medicine, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, People's Republic of China.
Abstract
Chemotherapy drugs such as cyclophosphamide (CTX), doxorubicin (DOX), and cisplatin (CIS) are widely used in the treatment of malignant tumors, including head and neck cancers, leukemia, ovarian cancer, and breast cancer. However, these drugs are frequently associated with severe side effects, particularly ovarian toxicity, which significantly compromises fertility and quality of life in female patients. Current research has revealed that chemotherapy associated ovarian damage(CAOD) involves a range of pathological and molecular mechanisms, including extracellular matrix(ECM) deposition, stromal fibrosis, ovarian vascular injury, DNA damage, redox imbalance, immune microenvironment dysregulation, and excessive activation of primordial follicles(PMFs). From a clinical perspective, embryo and oocyte cryopreservation, as well as ovarian tissue cryopreservation in appropriate patients, represent established fertility-preservation approaches, whereas ovarian-protective interventions such as GnRH agonists (GnRHa) remain subject to ongoing clinical evaluation. In contrast, stem cell therapy, antiapoptotic agents, antioxidants, and strategies targeting excessive follicle activation are predominantly supported by preclinical evidence and have not yet been established as routine clinical treatments. This article provides a narrative review of the major pathological features and molecular mechanisms of chemotherapy-induced ovarian damage, evaluates the limitations of existing prevention and treatment strategies, and aims to advance academic discourse in the field of CAOD prevention and treatment, while offering insights for future research.
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BibTeX
@article{qi2026chemotherapyassociated,
title = {{Chemotherapy-Associated Ovarian Damage: Pathological Mechanisms and Current Interventions.}},
author = {Wenlong Qi and Zhicheng Jia and Mengyu Shi and Xinxin Yang and Xinwei Sun and Haiying Zhou and Ying Guo},
journal = {International journal of women's health},
year = {2026},
month = oct,
doi = {10.2147/ijwh.s653166},
url = {https://europepmc.org/article/MED/42968847},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Chemotherapy-Associated Ovarian Damage: Pathological Mechanisms and Current Interventions.
AU - Wenlong Qi
AU - Zhicheng Jia
AU - Mengyu Shi
AU - Xinxin Yang
AU - Xinwei Sun
AU - Haiying Zhou
AU - Ying Guo
PY - 2026
DA - 2026/10/28
JO - International journal of women's health
DO - 10.2147/ijwh.s653166
UR - https://europepmc.org/article/MED/42968847
AB - Chemotherapy drugs such as cyclophosphamide (CTX), doxorubicin (DOX), and cisplatin (CIS) are widely used in the treatment of malignant tumors, including head and neck cancers, leukemia, ovarian cancer, and breast cancer. However, these drugs are frequently associated with severe side effects, particularly ovarian toxicity, which significantly compromises fertility and quality of life in female patients. Current research has revealed that chemotherapy associated ovarian damage(CAOD) involves a range of pathological and molecular mechanisms, including extracellular matrix(ECM) deposition, stromal fibrosis, ovarian vascular injury, DNA damage, redox imbalance, immune microenvironment dysregulation, and excessive activation of primordial follicles(PMFs). From a clinical perspective, embryo and oocyte cryopreservation, as well as ovarian tissue cryopreservation in appropriate patients, represent established fertility-preservation approaches, whereas ovarian-protective interventions such as GnRH agonists (GnRHa) remain subject to ongoing clinical evaluation. In contrast, stem cell therapy, antiapoptotic agents, antioxidants, and strategies targeting excessive follicle activation are predominantly supported by preclinical evidence and have not yet been established as routine clinical treatments. This article provides a narrative review of the major pathological features and molecular mechanisms of chemotherapy-induced ovarian damage, evaluates the limitations of existing prevention and treatment strategies, and aims to advance academic discourse in the field of CAOD prevention and treatment, while offering insights for future research.
SN - 1179-1411
ER -