This is the authors' abstract. We don't add key points for this paper.
This review focuses on the intricate molecular mechanisms and advancements of ferroptosis in Acute Myeloid Leukemia (AML) treatment. AML, an uncontrolled proliferation of undifferentiated myeloid precursor cells, demonstrates a high degree of chemotherapy resistance, resulting in poor prognosis. Ferroptosis, a distinct form of cell death involving iron accumulation and lipid peroxidation, has emerged as a promising therapeutic strategy. Herein, we dissect the oxidative-antioxidative mechanisms and iron death, highlighting the roles of the glutathione system and Fenton reaction. Furthermore, the association of lipid peroxidation with ferroptosis, as well as the advancements in AML research focusing on the XCT-GSH-GPX4 pathway and the interplay of autophagy and ferroptosis, are detailed. This comprehensive analysis underscores the potential of ferroptosis as a targeted therapeutic approach for AML.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: