Vascular Endothelial Growth Factor and Sleep Apnea: Clutching at Straws in the Night

Cherniack, E. Paul

doi:10.1159/000096835

Cited by 6 publications

(3 citation statements)

References 8 publications

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“…VEGF is thought to promote atherogenesis through endothelial cell proliferation, cell migration, and increased vascular permeability. 34 Previous clinical studies have shown higher levels of VEGF in OSA patients than in controls, 35,36 mainly as a result of hypoxia. Our results were limited by the great variability in VEGF in the sample, which prevented us from finding any differences between groups.…”

Section: Discussionmentioning

confidence: 95%

Impact of OSA on Biological Markers in Morbid Obesity and Metabolic Syndrome

Salord¹,

Gasa

Mayos³

et al. 2014

Journal of Clinical Sleep Medicine

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Section: Discussionmentioning

confidence: 95%

Impact of OSA on Biological Markers in Morbid Obesity and Metabolic Syndrome

Salord¹,

Gasa

Mayos³

et al. 2014

Journal of Clinical Sleep Medicine

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“…Patients with sleep apnea have increased plasma levels of VEGF [15,16,17,18,19]. Recent findings suggest that vascular function is impaired in OSA and that endothelial dysfunction may precede and predispose these patients to cardiovascular events [20,21,22,23,24].…”

Section: Introductionmentioning

confidence: 99%

Endothelial Function and Circulating Endothelial Progenitor Cells in Patients with Sleep Apnea Syndrome

Peña

Barceló²,

Barbé

et al. 2007

Respiration

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Background: Endothelial dysfunction and cardiovascular diseases are frequent in patients with obstructive sleep apnea (OSA). Circulating endothelial progenitor cells (EPCs) contribute to repair dysfunctional endothelium and have been related to increased cardiovascular risk. Objectives: We tested the hypothesis that the number of circulating EPCs may be altered in OSA patients. Methods: EPCs (CD34+ VEGF-R2+) were isolated and quantified from peripheral blood samples of OSA patients (n = 13) and healthy controls (n = 13) matched for age and sex. All subjects were free of any other known cardiovascular risk factors. The plasma levels of vascular endothelial growth factor (VEGF) were also determined, and the endothelium-dependent and endothelium-independent vascular function was assessed in all subjects. Results: Patients with OSA had lower levels of EPCs (p < 0.05) and higher plasma levels of VEGF (p < 0.05) than controls. Endothelial function was not different between OSA and controls. Conclusions: Patients with OSA free of any other known cardiovascular risk factor show a reduced number of circulating EPCs and an increase in plasma VEGF levels. These alterations may contribute to future endothelial dysfunction in these patients.

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“…Numerous reports have shown that plasma levels of VEGF are elevated in patients with OSA 41,99,111,123. VEGF expression is markedly increased in patients with OSA, largely because of the effects of HIF-1 on VEGF transcription 124.…”

Section: Pathogenetic Mechanisms Of Osa and The Effects Of Osa On Epcmentioning

confidence: 99%

Obstructive sleep apnea and endothelial progenitor cells

Wang¹,

Wu²,

Feng³

et al. 2013

PPA

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BackgroundObstructive sleep apnea (OSA) occurs in 4% of middle-aged men and 2% of middle-aged women in the general population, and the prevalence is even higher in specific patient groups. OSA is an independent risk factor for a variety of cardiovascular diseases. Endothelial injury could be the pivotal determinant in the development of cardiovascular pathology in OSA. Endothelial damage ultimately represents a dynamic balance between the magnitude of injury and the capacity for repair. Bone marrow–derived endothelial progenitor cells (EPCs) within adult peripheral blood present a possible means of vascular maintenance that could home to sites of injury and restore endothelial integrity and normal function.MethodsWe summarized pathogenetic mechanisms of OSA and searched for available studies on numbers and functions of EPCs in patients with OSA to explore the potential links between the numbers and functions of EPCs and OSA. In particular, we tried to elucidate the molecular mechanisms of the effects of OSA on EPCs.ConclusionIntermittent hypoxia cycles and sleep fragmentation are major pathophysiologic characters of OSA. Intermittent hypoxia acts as a trigger of oxidative stress, systemic inflammation, and sympathetic activation. Sleep fragmentation is associated with a burst of sympathetic activation and systemic inflammation. In most studies, a reduction in circulating EPCs has emerged. The possible mechanisms underlying the decrease in the number or function of EPCs include prolonged inflammation response, oxidative stress, increased sympathetic activation, physiological adaptive responses of tissue to hypoxia, reduced EPC mobilization, EPC apoptosis, and functional impairment in untreated OSA. Continuous positive airway pressure (CPAP) therapy for OSA affects the mobilization, apoptosis, and function of EPCs through preventing intermittent hypoxia episodes, improving sleep quality, and reducing systemic inflammation, oxidative stress levels, and sympathetic overactivation. To improve CPAP adherence, the medical staff should pay attention to making the titration trial a comfortable first CPAP experience for the patients; for example, using the most appropriate ventilators or proper humidification. It is also important to give the patients education and support about CPAP use in the follow-up, especially in the early stage of the treatment.

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Vascular Endothelial Growth Factor and Sleep Apnea: Clutching at Straws in the Night

Cited by 6 publications

References 8 publications

Impact of OSA on Biological Markers in Morbid Obesity and Metabolic Syndrome

Impact of OSA on Biological Markers in Morbid Obesity and Metabolic Syndrome

Endothelial Function and Circulating Endothelial Progenitor Cells in Patients with Sleep Apnea Syndrome

Obstructive sleep apnea and endothelial progenitor cells

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