Levels of vascular endothelial growth factor are elevated in patients with obstructive sleep apnea–hypopnea syndrome

Imagawa, Shigehiko; Yamaguchi, Yuji; Higuchi, M.; Neichi, Tomohiro; Hasegawa, Yoshinori; Mukai, Harumi Y.; Suzuki, Norio; Yamamoto, Masayuki; Nagasawa, Toshiro

doi:10.1182/blood.v98.4.1255

Cited by 93 publications

(84 citation statements)

References 18 publications

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“…Although VEGF has been demonstrated in various types of cells to be stimulated by hypoxia (5), in respiratory diseases with chronic hypoxic manifestation, data about VEGF regulation are conflicting. Several investigations in obstructive sleep apnea (10,15,43,46) and cystic fibrosis (29) revealing an increase in serum VEGF have been criticized, because VEGF is released from activated platelets during the in vitro clotting process (12,17,18). On the other hand, measuring VEGF in plasma (22) and in bronchoalveolar lavage fluid (31) yielded the same result.…”

mentioning

confidence: 63%

Acute hypoxia decreases plasma VEGF concentration in healthy humans

Oltmanns

Gehring

Rudolf

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders, such as insulin, glucose concentrations, or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind crossover study design, we induced hypoxia for 30 min by decreasing oxygen saturation to 75% (vs. normoxic control) in 14 healthy men. Plasma VEGF concentration was determined at baseline, immediately after hypoxia had ended, and after a further 150 min. Levels of its soluble (s)Flt-1 receptor were assessed at baseline and at the end of the clamp. In parallel, catecholamine and cortisol levels were monitored. To investigate potential effects of glucose administration on the release of VEGF, we performed a third session, reducing glucose infusion for 30 min while serum insulin was held stable thereby inducing hypoglycemia. Hypoxia decreased VEGF levels compared with the normoxic control ( P < 0.05). VEGF concentrations increased during hypoglycemia ( P < 0.02) but were comparable to the normoglycemic control at the end of the clamp ( P > 0.80). sFlt-1 receptor concentration remained unchanged during hypoxia and hypoglycemia compared with control (both P > 0.4). Epinephrine concentration ( P < 0.01) increased upon hypoxia, whereas norepinephrine and cortisol did not change. Contrary to in vitro studies, in healthy humans hypoxia decreases plasma VEGF concentration, suggesting that systemic VEGF concentration may be differently regulated than the expression on cellular basis.

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confidence: 63%

Acute hypoxia decreases plasma VEGF concentration in healthy humans

Oltmanns

Gehring

Rudolf

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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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: 99%

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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“…It has been reported that serum VEGFlevels are significantly higher in patients with polysomnographically confirmed OSAS(AHI>15 and AI>5 in adults and children, respectively) than in patients with mild disease or no disease (18,19 cells, which appears to play a pivotal role in physiological and pathological angiogenesis (13). VEGFhas been shown to be an important factor in the pathogenesis of vascularrelated diseases, including the growth of tumors, vascular dysfunction in diabetes mellitus, and atherosclerosis of the coronary arteries (13,27,28).…”

Section: Discussionmentioning

confidence: 99%