Figures & data
Figure 1 A simplified model where an HSC or early hematopoietic precursor develops a fault in autophagy/mitophagy (1) which leads to the build up of damaged mitochondria. These in turn cause an increase in metabolic by-products, including ROS (2) which result in cellular damage including genetic instability and more mitochondrial damage. A loss of quiescence results, along with both increased apoptosis (3) and proliferation (4) in an MDS phenotype. Oncogenic mutations may result in transformation and AML (5).
