Abstract:Acute myeloid leukemia (AML) is a hematologic malignancy with a complex pathogenesis involving the dysregulation of multiple genes and signaling pathways. In recent years, ferroptosis, as a novel form of regulated cell death, has become a research hotspot. This review summarizes the research progress on ferroptosis in AML, exploring the mechanisms, regulatory factors, and its role in the onset and progression of AML, while discussing the potential of ferroptosis as a therapeutic target for AML. Current studies indicate that ferroptosis plays a pivotal role in AML by modulating pathways such as iron metabolism, oxidative stress, and autophagy, thereby influencing the survival and death of leukemic cells. The induction of ferroptosis might represent a novel therapeutic strategy for AML, providing theoretical support for the development of new treatment approaches. However, the precise role of ferroptosis in AML remains unclear and requires further investigation. Additionally, how to effectively induce ferroptosis without damaging normal cells is a critical challenge that must be addressed in future research. Therefore, in-depth studies on ferroptosis are expected to enhance the understanding of AML pathogenesis and offer new possibilities for therapeutic interventions.