Cisplatin, a vital chemotherapy drug for solid malignant tumors, can detrimentally affect ovarian health and fertility in premenopausal patients with cancer. Currently, effective strategies to mitigate cisplatin-induced ovarian damage remain limited. Several studies have highlighted the potential of metformin as an anticancer agent with anti-aging properties and other health benefits. Hence, the present study established an animal model to investigate the impact of metformin on cisplatin-induced ovarian damage, elucidating its mechanisms using bulk RNA sequencing analysis and Western blotting. Our study findings demonstrate that metformin significantly prevents the decline in cisplatin-induced ovarian reserve, maintaining anti-müllerian hormone (AMH) and estradiol (E2) levels. Moreover, metformin may effectively improve cisplatin-induced ovarian fibrosis and granulosa cell pyroptosis through the ROS/TXNIP/NLRP3 pathway. In summary, our study indicates that metformin holds promise in alleviating cisplatin-induced ovarian damage, offering a potential avenue to preserve female fertility during chemotherapy.

Pelvic organ prolapse (POP) is a benign disease characterized by the descent of pelvic organs due to weakened pelvic floor muscles and fascial tissues. Primarily affecting elderly women, POP can lead to various urinary and gastrointestinal tract symptoms, significantly impacting their quality of life. The pathogenesis of POP predominantly involves nerve–muscle damage and disorders in the extracellular matrix metabolism within the pelvic floor. Recent studies have indicated that genetic factors may play a crucial role in this condition. Focusing on linkage analyses, single-nucleotide polymorphisms, genome-wide association studies, and whole exome sequencing studies, this review consolidates current research on the genetic predisposition to POP. Advances in epigenetics are also summarized and highlighted, aiming to provide theoretical recommendations for risk assessments, diagnoses, and the personalized treatment for patients with POP.

The ovary holds a significant role as a reproductive endocrine organ in women, and its aging process bears implications such as menopause, decreased fertility, and long-term health risks including osteoporosis, cardiovascular disorders, and cognitive decline. The phenomenon of oxidative stress is tightly linked to the aging metabolic processes. More and more studies have demonstrated that oxidative stress impacts both physiologic and pathologic ovarian aging, and the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays a crucial role in regulating the antioxidant response. Furthermore, various therapeutic approaches have been identified to ameliorate ovarian aging by modulating the Nrf2 pathway. This review summarizes the important role of the Nrf2/ Kelch-like ECH-associated protein 1 (Keap1) signaling pathway in regulating oxidative stress and influencing ovarian aging. Additionally, it highlights the therapeutic strategies aimed at targeting the Nrf2/Keap1 pathway.