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.
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.
Radiotelemetric and genetic studies of peripheral tissue response show that a peripheral tissue can dynamically alter cardiovascular adaptation to changes in environmental oxygen.