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.

Acute intermittent hypoxia is a noninvasive approach that enhances corticospinal function in humans, likely through alterations in corticospinal-motoneuronal synaptic transmission.

Targeting STAT3 provides a potential therapeutic strategy for obstructive sleep apnea-related fibrotic heart disease mediated by TSP1.

Glutamatergic–cholinergic neurons in the postinspiratory complex are critical for swallow motor patterning and the coordination of swallow and breathing, which is disrupted by chronic intermittent hypoxia, a condition seen in many disorders associated with dysphagia and aspiration pneumonia.

A single neonatal inflammatory event induces long-term impairments in two forms of adult respiratory motor plasticity, an important aspect of the control of breathing for compensation after injury or disease.

The long-distance flight of locusts is greatly facilitated by a muscle-abundantly expressed Hif-1α splice variant, which remains active in normoxia and scavenges flight-induced reactive oxygen species by upregulating the expression of DJ-1 (PARK 7).

Expression of Bisphosphoglycerate mutase, a key enzyme affecting the release of oxygen from hemoglobin, is augmented in the murine placenta challenged by gestational hypoxia in mice while its expression is attenuated in placenta of human FGR.

Neural progenitors reside in relative low oxygen in the subgranular zone (SGZ), and the higher tissue oxygen levels that these cells must face as they migrate away from the hypoxic areas and differentiate appear to cause oxidative damage and an early phase of cell death.

The repression of HIF-1 plays a central role in mitochondrial reactive oxygen species (ROS) overproduction and subsequent tissue damage in diabetes, which is mediated by increased mitochondrial respiration, making HIF-1 signaling an attractive therapeutic target for diabetes complications.

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