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.