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The subcellular localization of the prolyl hydroxylase oxygen sensor in C. elegans neurons is regulated by p38 MAP kinase signaling.

The interplay between the transcriptional co-regulators YAP1/TAZ and the hypoxia-controlled transcription factor HIF1α differentially regulates endothelial cell behavior in the hypoxic environment of bone compared to other organs.

Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.

Mouse models in which hypoxia can be genetically triggered in retinal pigmented epithelial cells show that hypoxia-induced metabolic stress alone can lead to photoreceptor atrophy/dysfunction.

Neonatal hyperoxia abrogates the circadian protection from influenza infection in recovered adults.

Atoh1 promotes the development of two different neural circuits involved in hypoxic and hypercapnic respiratory responses that together are essential for neonatal respiratory drive and survival.

The immediate response of the brain to a sudden, harmful drop in oxygen supply is the addition of SUMO proteins to sodium ion channels in neurons, increasing their activity.

The survival and growth of solid tumor cells in hypoxia is dependent on fatty acid storage in triglyceride lipid droplets promoted by HIG2.

Local tissue hypoxia follows seizures, is responsible for postictal behavioural dysfunction rather than the seizures per se and can be treated.

The current findings address the redox regulation of hypoxia inducible factor 1α (HIF1α) stability in hypoxia by showing that cytosolic, mitochondrial or lipid ROS are not necessary for HIF1α stabilization in hypoxia.