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Article Abstract
Cervical cancer (CC) exerts a considerable impact on women's health worldwide and presents persistent challenges to conventional therapeutic strategies due to its propensity for distant metastasis, postoperative recurrence, and variable drug resistance. Ferroptosis, a recently identified type of programmed cell death, offers promising potential for a therapeutic approach for CC. This paper reviews the regulatory processes involved in ferroptosis, including the sequential events leading to cell membrane rupture via lipid peroxidation and the changes in ferroptosis sensitivity as cervical cells progress from a healthy to a malignant condition. Additionally, the dynamic relationship between ferroptosis and CC transformation driven by high-risk HPV (HR-HPV) infection is examined, with a particular focus on how HR-HPV E6/E7 proteins influence ferroptosis sensitivity. By examining the factors associated with ferroptosis, this review provides insights into CC progression and prognosis. Furthermore, therapeutic strategies targeting ferroptosis are discussed, offering novel perspectives for effective treatment options for CC.
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