[Aberrant mitochondrial dynamics in myeloid neoplasms]

Growing evidence has revealed that mitochondria are not merely bioenergetic organelles but also critical regulators of inflammation, cell death, and stem cell maintenance. Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are myeloid malignancies that arise from hematopoietic stem and progenitor cells harboring genetic alterations; however, their fundamental disease phenotypes are distinct. Notably, hematopoietic stem and progenitor cells in MDS, which are characterized by chronic inflammation and ineffective hematopoiesis, exhibit excessive mitochondrial fragmentation independent of the underlying mutational profile. In contrast, AML, a malignancy driven primarily by uncontrolled proliferation, is associated with mitochondrial fusion and an increase in mitochondrial mass. These distinct mitochondrial dynamics appear to reflect disease-specific biological demands rather than incidental cellular abnormalities. This review focuses on the differences in mitochondrial dynamics and function between MDS and AML and discusses how these mitochondrial alterations contribute to the pathogenesis of myeloid neoplasms.