Hypobaric hypoxia exposure initiates splenic ferroptosis, reducing red pulp macrophages and exacerbating high-altitude polycythemia by impairing erythrophagocytosis and increasing red blood cell retention.

Previous studies and emerging data on pseudohypoxic diseases suggest that the complex phenotypic spectrum of VHL disease is due to the extent of HIF pathway deregulation in susceptible cell types and not by other purported substrates or functions of pVHL.

A combination of composite-likelihood and gene network-based methods to investigate the impact of Denisovan introgression on the evolution of complex (i.e., polygenic) adaptive traits in high-altitude populations of Tibetan/Sherpa ancestry.

Genetic and physiological analyses demonstrate the essential role of the transcription factor HIF-2alpha in the sympathetic nervous system control of the ventilatory response to hypoxia.

A survey of oxygen-dependent enzymes suggests new candidates for oxygen sensors, expanding potential mechanisms underlying hypoxia-related adaptations or diseases in humans.