Key result
Chronic intermittent hypoxia induced by obstructive sleep apnea-hypopnea syndrome promotes the development of atherosclerosis via inflammation, oxidative stress, and vascular endothelial injury.
This review summarizes the pathophysiological mechanisms by which chronic intermittent hypoxia in obstructive sleep apnea promotes the development of atherosclerosis.
OSAHS-related hypoxia may promote atherosclerosis; leaves open causal confirmation and need for interventional trials.
The morbidity and mortality of obstructive sleep apnea-hypopnea syndrome (OSAHS) are regarded as consequences of its adverse effects on the cardiovascular system. Chronic intermittent hypoxia (CIH) induced by OSAHS can result in vascular endothelial injury, thus promoting development of atherosclerosis (AS). Studies have shown that CIH is an independent risk factor for the occurrence and development of AS, but the underlying mechanism remains unclear. Here, we review clinical and fundamental studies reported during the last 10 years on the occurrence and development of AS mediated by CIH, focusing on inflammation, oxidative stress, insulin resistance, cell apoptosis, vascular endothelial injury, platelet activation, and neuroendocrine disorders. This review will offer current evidence and perspective to researchers for the development of effective intervention strategies for OSAHS-related cardiocerebrovascular diseases.
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Ma et al. (2016) conducted a review in Obstructive sleep apnea-hypopnea syndrome (OSAHS) and atherosclerosis. Chronic intermittent hypoxia (CIH) was evaluated on Occurrence and development of atherosclerosis. Chronic intermittent hypoxia induced by obstructive sleep apnea-hypopnea syndrome promotes the development of atherosclerosis via inflammation, oxidative stress, and vascular endothelial injury.
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