期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 130, 期 10, 页码 5042-5051出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI137560
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资金
- NIH (National Heart, Lung, and Blood Institute) [P01-HL-44454]
Intermittent hypoxia (IH) is a hallmark manifestation of obstructive sleep apnea (OSA), a widespread disorder of breathing. This Review focuses on the role of hypoxia-inducible factors (HIFs) in hypertension, type 2 diabetes (T2D), and cognitive decline in experimental models of IH patterned after O-2 profiles seen in OSA. IH increases HIF-1 alpha and decreases HIF-2 alpha protein levels. Dysregulated HIFs increase reactive oxygen species (ROS) through HIF-1-dependent activation of pro-oxidant enzyme genes in addition to reduced transcription of antioxidant genes by HIF-2. ROS in turn activate chemoreflex and suppress baroreflex, thereby stimulating the sympathetic nervous system and causing hypertension. We also discuss how increased ROS generation by HIF-1 contributes to IH-induced insulin resistance and T2D as well as disrupted NMDA receptor signaling in the hippocampus, resulting in cognitive decline.
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