Ferroptosis determinants – potential predictors and therapeutic targets for acute myeloid leukemia

Ferroptosis (FP) is a type of non-apoptotic programmed cell death associated with iron-dependent lipid peroxidation. FP is characterized by a decrease in the activity of glutathione peroxidase 4, which is necessary for the suppression of lipid peroxidation, accumulation of redox-active iron and oxidation of cell membrane phospholipids containing polyunsaturated fatty acids. FP plays a central role in the mechanisms of human aging, regulating degeneration – the main cause of tissue damage and organ failure. FP makes a significant contribution to the development of age-related pathologies, including neurodegenerative conditions, cardiovascular diseases, and cancer. Of particular interest is the participation of FP in the pathogenesis of age-related oncological diseases, including acute myeloid leukemia (AML). Previous studies show that FP largely regulates the sensitivity of AML cells to chemotherapeutic drugs, and some of the FP-related genes play a vital role in AML oncogenesis. In addition, there is considerable interest in investigating the effect of immune infiltration on FP and the prognosis of AML. Thus, an in-depth study of the unique mechanism of FP in AML may provide new insights into the diagnosis and treatment of this disease. This review analyzes the main regulatory molecular mechanisms of FP and the relationship of FP with the occurrence and development of AML. In addition, recent advances in the study of the role of FP in the prognosis and therapy of AML are summarized.