Targeting cellular senescence in cervical Cancer: a novel pathway to preserve reproductive potential

Cervical cancer is a major global health concern, especially among women of reproductive age, where standard treatments often compromise fertility. Cellular senescence has a dual role in cervical cancer, acting as both a tumor suppressor and promoter through the senescence-associated secretory phenotype (SASP). Human Papillomavirus (HPV) infection, DNA damage, and oxidative stress trigger senescence, leading to SASP-mediated inflammation, tumor progression, and therapy resistance. Targeting senescence offers promising therapeutic opportunities. Senolytics selectively eliminate senescent cells, while senostatics suppress the SASP, improving the tumor microenvironment and enhancing traditional therapies. Telomerase reactivation and epigenetic modulation represent additional strategies to modulate senescence-associated phenotypes. Fertility-preserving treatments, such as radical trachelectomy, combined with senescence-targeting therapies, can expand options for reproductive-age patients, minimizing oncologic risks while maintaining reproductive potential. This review highlights the mechanisms of senescence in cervical cancer and explores novel pathways to target senescent cells, focusing on fertility preservation. Incorporating senescence-targeting strategies with conventional and fertility-sparing treatments may care for young patients, balancing oncologic efficacy with quality of life. Future research and clinical trials are essential to validate these approaches and optimize protocols for widespread clinical application.