Measurements of bar-headed geese flying in a wind tunnel in hypoxia reveal that these birds sustain aerobic flight at high altitude via a reduction in metabolism.

Animal survival in hypoxia requires the classical hypoxia-inducible factor (HIF) signalling pathway, but in the nematode worm C. elegans, a new signalling pathway involving the nuclear receptor NHR-49/PPARalpha is as important for hypoxia survival as the HIF pathway.

In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.

Under hypoxic stress, when cellular demand for energy relies entirely on glycolysis, the machinery for glycolysis binds RNA and phase separates into G bodies, leading to enhanced glycolysis rates.

RNA profiles from lungs of mice exposed to intermittent hypoxia shared similarity with gene expression changes in human lung from patients with pulmonary diseases, including pulmonary hypertension, COPD, and asthma.

Evolutionarily conserved hypoxic stress response genes are depleted for association with expression quantitative trait loci.

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation of MYC signaling pathways.

LncRNA Neat1, with paraspeckle proteins, controls translational induction of (lymph)angiogenic and cardioprotective factors by the IRES-dependent mechanism in mouse cardiomyocytes submitted to hypoxia.

HCAR1 knockout mice are unable to initiate brain tissue repair after a hypoxic-ischemic injury.

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