期刊
ANTIOXIDANTS
卷 10, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/antiox10060986
关键词
ferroptosis; Eprenetapopt; Erastin; GPX4; glutathione (GSH); iron; oxidative stress; NRF2
资金
- National Health and Medical Research Council (NMHRC) [APP1120293]
- Department of Health and Human Services acting through the Victorian Cancer Agency Fellowship [MCRF16002]
- Australian Research Training Program (RTP) Scholarship
Ferroptosis, a form of cell death characterized by lipid peroxidation and iron accumulation, has shown potential as an alternative therapeutic strategy for destroying tumors. Despite extensive research on its molecular mechanisms, translating this knowledge into clinical compounds remains a challenge. This perspective elaborates on leveraging ferroptosis in the clinic, discussing therapeutic windows, tumor sensitivity, conventional therapeutics, and strategies to enhance ferroptosis.
A critical hallmark of cancer cells is their ability to evade programmed apoptotic cell death. Consequently, resistance to anti-cancer therapeutics is a hurdle often observed in the clinic. Ferroptosis, a non-apoptotic form of cell death distinguished by toxic lipid peroxidation and iron accumulation, has garnered substantial attention as an alternative therapeutic strategy to selectively destroy tumours. Although there is a plethora of research outlining the molecular mechanisms of ferroptosis, these findings are yet to be translated into clinical compounds inducing ferroptosis. In this perspective, we elaborate on how ferroptosis can be leveraged in the clinic. We discuss a therapeutic window for compounds inducing ferroptosis, the subset of tumour types that are most sensitive to ferroptosis, conventional therapeutics that induce ferroptosis, and potential strategies for lowering the threshold for ferroptosis.
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