Fig. 8: Schematic representation of the consequences of the early Aif ablation in the hematopoietic cells

The loss of AIF in the hematopoietic cells resulted in a defective mitochondrial OXPHOS that was characterized by ΔΨm loss, high ROS generation, and drop in ATP levels. These alterations provoke pleiotropic consequences in neonatal and adult AIF−/Y mice, including a progressive pancytopenia and T-cell, B-cell, and erythroid developmental defaults. BM cells and thymocytes utilize different adaptive metabolic mechanisms: BM cells counterbalance the AIF-mediated OXPHOS dysfunction by the stimulation of mitochondrial biogenesis and a shift towards anaerobic glycolysis, whereas thymocytes favor the fatty acid metabolism