[Recent advances in the study of potential mitochondria-related therapeutic targets in acute myeloid leukemia]

Acute myeloid leukemia (AML), one of the most common types of leukemia, is characterized by its high malignancy and rapid progression with a 5-year survival rate of less than 30%. The incidence and mortality rates of AML are increasing with age. Over the past few decades, progress in AML treatment has been relatively slow. While traditional approaches such as chemotherapy and hematopoietic stem cell transplantation have significant limitations including treatment toxicity and chemotherapy resistance, recent advancements in the in-depth study of AML mechanisms have made targeted therapy a new option for AML treatment. Metabolic reprogramming is one of the key features of cancer, and mitochondrial dysfunction has been widely studied in various cancers. Mitochondrial dysfunction is prevalent in AML cells and closely associated with the development of AML. The AML cells exhibit significant differences from normal hematopoietic cells in energy metabolism, autophagy, apoptosis, and other aspects. Given that mitochondria are at the core of cellular energy metabolism, inhibiting pathways related to mitochondrial function holds significant potential for AML treatment. This review aims to explore recent advances on the role of mitochondrial dysfunction in AML cell survival, potential therapeutic targets in mitochondria, and related targeted drugs, aiming to provide ideas for the development of targeted therapies for AML.