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Hypoxia-inducible factors and obstructive sleep apnea
The Journal of Clinical Investigation
|July 31, 2020
Summary
Intermittent hypoxia in sleep apnea disrupts hypoxia-inducible factors (HIFs), increasing oxidative stress. This leads to hypertension, type 2 diabetes, and cognitive decline in experimental models.
Area of Science:
- Physiology
- Pathophysiology
- Molecular Biology
Background:
- Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH).
- Hypoxia-inducible factors (HIFs) play a critical role in cellular response to oxygen levels.
- Dysregulation of HIFs is implicated in various OSA-related comorbidities.
Purpose of the Study:
- To review the role of HIFs in experimental models of IH relevant to OSA.
- To examine the impact of IH-induced HIF dysregulation on hypertension, type 2 diabetes (T2D), and cognitive decline.
Main Methods:
- Review of experimental studies modeling IH with OSA-like oxygen profiles.
- Analysis of HIF-1α and HIF-2α protein level changes under IH conditions.
- Investigation of reactive oxygen species (ROS) generation and downstream signaling pathways.
Main Results:
- IH alters HIF-1α and HIF-2α protein levels.
- Dysregulated HIFs increase ROS production via HIF-1-dependent pathways and reduced antioxidant gene transcription by HIF-2.
- Increased ROS activates chemoreflex, suppresses baroreflex, stimulates sympathetic nervous system, leading to hypertension.
Conclusions:
- IH-induced HIF dysregulation contributes to hypertension through sympathetic nervous system activation.
- Increased ROS generation by HIF-1 promotes insulin resistance and T2D.
- Disrupted NMDA receptor signaling in the hippocampus due to ROS contributes to cognitive decline.
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