Advances in pharmaceutical protection against radiation-induced injury in the female reproductive system: from molecular pathways to clinical practice
10.12025/j.issn.1008-6358.2025.20250839
- VernacularTitle:女性生殖系统辐射损伤的药物防护进展：从分子通路到临床实践
- Author:
Bendong LI
1
;
Shengyun CAI
1
Author Information
1. Department of Obstetrics and Gynecology, the First Affiliated Hospital of Naval Medical University, Shanghai 200433, China.
- Publication Type:Review
- Keywords:
ionizing radiation;
ovarian function impairment;
reproductive function;
fertility preservation;
pharmaceutical protection
- From:
Chinese Journal of Clinical Medicine
2025;32(6):1053-1067
- CountryChina
- Language:Chinese
-
Abstract:
Ionizing radiation impairs ovarian function by inducing DNA double-strand breaks, oxidative stress, and inflammatory cascades, leading to primordial follicle depletion and premature ovarian insufficiency (POI). Core mechanisms involve ATM/p53-mediated DNA damage response, granulosa cell apoptosis triggered by a sharp increase in reactive oxygen species/reactive nitrogen species (ROS/RNS), and Toll-like receptor (TLR)/NF-κB-driven chronic inflammation. Currently, only amifostine and palifermin are internationally approved radioprotective agents, yet they exhibit significant limitations including severe toxicity, narrow indications, and lack of conclusive evidence for ovarian protection. Investigational agents like the natural antioxidant melatonin require further clinical validation for ovarian radioprotection. Emerging strategies, such as TLR5 agonists, mitochondrial-targeted agents, and targeted drug delivery systems, provide novel directions for mitigating radiation-induced ovarian injury. This review synthesizes key pathways of radiation-induced ovarian damage, explores cutting-edge mechanisms, and highlights promising novel radioprotective agents. The proposed synergistic “epigenetic regulation + immunomodulation” strategy embodies a paradigm shift from passive mitigation to active precision protection against ovarian radiation damage.
