ArticleJournal of translational medicine2026
Endothelial glycocalyx perturbation in obstructive sleep apnea is associated with repetitive hypoxemia and immunothrombotic endothelial dysfunction.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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15 authors.
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Abstract
backgroundObstructive sleep apnea (OSA) is associated with cardiovascular disease. The endothelial glycocalyx (eGCX) is a shear-sensitive intravascular barrier. The relevance of OSA and intermittent hypoxia (IH) for eGCX perturbation and cardiovascular disease in humans remains unclear.
methodsIn a prospectively recruited observational cohort with cross-sectional biomarker analysis in men (n = 60), polysomnography quantified apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and hypoxic burden (HB). Using single-time-point plasma sampling, eGCX glycosaminoglycans hyaluronan (HA) and heparan sulfate (HS) and the proteoglycan syndecan-1 (SDC-1) were related to OSA severity and repetitive hypoxemia, including multivariable adjustment for cardiometabolic, inflammatory, and renal determinants. Plasma proteomics defined pathways associated with OSA and HA/HS. Shear-matured primary human endothelial cells were exposed to OSA-characteristic IH cycles under arterial flow to assess eGCX structure, oxidative stress, nitric oxide (NO) signaling, thromboinflammatory status, and antioxidant treatment with N-acetylcysteine.
resultsPlasma HA and HS were higher in OSA than in non-OSA individuals and increased stepwise with disease severity, tracking AHI, ODI, and HB. These associations persisted in multivariable analyses adjusting for age, BMI, hypertension, hs-CRP, fasting glucose, and eGFR. Plasma SDC-1 did not differ between groups and remained non-associated in adjusted analyses. Proteomics revealed enrichment of inflammatory, coagulation, and oxidative stress-related pathways that strengthened with increasing OSA burden and higher HA/HS levels. Experimentally, IH caused loss of endothelial surface HA/HS with increased shedding, increased reactive oxygen species, reduced redox capacity, impaired NOS3/eNOS signaling and reduced NO bioavailability. IH or enzymatic eGCX digestion each enhanced monocyte and platelet adhesion, tissue factor expression, and fibrin deposition under shear, while N-acetylcysteine attenuated oxidative stress and partially restored surface HA expression.
conclusionsIntegrated patient and IH-model data show that OSA severity and repetitive hypoxemia are associated with circulating markers consistent with eGCX perturbation, while the endothelial IH model supports induction of oxidative-inflammatory stress and a proadhesive, prothrombotic phenotype by intermittent hypoxia. Together, circulating HA and HS emerge as candidate biomarkers associated with OSA-related eGCX perturbation, warranting further evaluation in longitudinal and interventional studies of eGCX-stabilizing adjunct therapies. These findings derive from an all-male cohort and require validation in women and more diverse populations.
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