HIF1A and pulmonary arterial hypertension: In PAH and cancer, mitochondrial metabolism and redox signaling are reversibly disordered, creating a pseudohypoxic redox state characterized by normoxic decreases in ROS, a shift from oxidative to glycolytic metabolism, and hypoxia-inducible factor-1α (HIF-1α) activation (190, 191), which lead to sustained ATP production, uncontrolled cell growth and cellular resistance to apoptosis (192–194).