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Updated: Aug 13, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Hypoxia-sensitive molecules may modulate the development of atherosclerosis in sleep apnoea syndrome
Motonori Hayashi1, Keisaku Fujimoto, Kazuhisa Urushibata
1First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Objectives:
Obstructive sleep apnoea hypopnoea syndrome (OSAHS) is associated with increased morbidity and mortality due to cardiovascular disease. In order to examine the association between OSAHS and cardiovascular disease, this study measured hypoxia-inducible and atherosclerosis-associated molecules in the peripheral blood.
Methods:
In this study peripheral blood was obtained early in the morning from 60 consecutive male patients with OSAHS (AHI > or =10 events/h) and 30 male control subjects without OSAHS (AHI <5 events/h). Serum levels of heat shock protein-70 (Hsp-70), tissue factor (TF), monocyte chemotactic protein-1 (MCP-1), highly sensitive C-reactive protein (hs-CRP), hepatocyte growth factor and plasma vascular endothelial growth factor were measured and their relationship with severity and hypoxaemia in OSAHS examined.
Results:
Serum hs-CRP, TF, MCP-1 and Hsp-70 levels were significantly higher in OSAHS compared with control subjects. Categorization of the patients into mild (10 < or = AHI < 30 events/h), moderate (30 < or = AHI < 60 events/h) and severe (AHI > or = 60 events/h) OSAHS subgroups showed that serum levels of hs-CRP, TF and Hsp-70 increased with severity. The hs-CRP, TF, MCP-1 and Hsp-70 levels in the non-obese OSAHS group were also significantly higher than those in the control group whereas there was no difference in BMI between the two groups. Repetitive hypoxaemia significantly correlated with hs-CRP, TF and Hsp-70 levels and appeared to be a significant determinant for these molecules.
Conclusions:
These findings suggest that CRP, TF and Hsp-70 may be upregulated by repetitive hypoxaemia in OSAHS and may be involved in the development of the atherogenic process in OSAHS.
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