Shenzhen Key Laboratory of Fertility Regulation, Reproductive Medicine Center, The University of Hong Kong-Shenzhen Hospital, Shenzhen, PR China.
Department of Breast and Thyroid Surgery, Peking University Shenzhen Hospital, Shenzhen, PR China.
Hum Fertil (Camb). 2023 Oct;26(4):887-900. doi: 10.1080/14647273.2023.2275764. Epub 2023 Dec 17.
More than 9.2 million women worldwide suffer from cancer, and about 5% of them are at reproductive age. Chemotherapy-induced impairment of fertility affects the quality of life of these women. Several chemotherapeutic agents have been proven to cause apoptosis and autophagy by inducing DNA damage and cellular stress. Injuries to the ovarian stroma and micro-vessel network are also considered as pivotal factors resulting in ovarian dysfunction induced by chemotherapeutic agents. Primordial follicle pool over-activation may also be the mechanism inducing damage to the ovarian reserve. Although many studies have explored the mechanisms involved in chemotherapy-induced reproductive toxicity, the exact molecular mechanisms have not been elucidated. It is essential to understand the mechanisms involved in ovarian damage, in order to develop potential protective treatments to preserve fertility. In this article, we reviewed the current knowledge on the mechanism of chemotherapy-induced ovarian damage and possible protective strategies that prevent the ovary from such damages.
全世界有超过 920 万名女性患有癌症,其中约 5%处于生育年龄。化疗引起的生育能力损害影响了这些女性的生活质量。几种化疗药物已被证明通过诱导 DNA 损伤和细胞应激导致细胞凋亡和自噬。卵巢基质和微血管网络的损伤也被认为是导致化疗药物引起卵巢功能障碍的关键因素。原始卵泡池过度激活也可能是导致卵巢储备损伤的机制。尽管许多研究已经探讨了化疗引起的生殖毒性的相关机制,但确切的分子机制尚未阐明。了解卵巢损伤的相关机制对于开发潜在的保护治疗以保留生育能力至关重要。在本文中,我们综述了化疗引起的卵巢损伤的机制以及可能预防卵巢损伤的保护策略。