Endothelial Dysfunction and Cardiovascular Risk in Obstructive Sleep Apnea: A Review Article
dc.contributor.author
dc.date.accessioned
2022-10-06T06:33:12Z
dc.date.available
2022-10-06T06:33:12Z
dc.date.issued
2022-04-05
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dc.description.abstract
Obstructive sleep apnea (OSA) is a respiratory condition during sleep caused by repeated pauses in breathing due to upper airway obstruction. It is estimated that OSA affects 30% of the population, but only 10% are well diagnosed due to the absence of a well-defined symptomatology and poor screening tools for early diagnosis. OSA is associated to an endothelial dysfunction inducing several biological responses such as hypoxia, hypercapnia and oxidative stress, among others. OSA also triggers respiratory, nervous, metabolic, humoral and immunity system activations that increase the possibility of suffering a cardiovascular (CV) disease. In this review, we expose different studies that show the relationship between OSA and endothelial dysfunction and its association with CV pathologies like hypertension, and we define the most well-known treatments and their limitations. Additionally, we describe the potential future directions in OSA research, and we report clinical features such as endothelial progenitor cell alterations that could act as biomarkers for the development of new diagnostic tools and target therapies
dc.format.mimetype
application/pdf
dc.language.iso
eng
dc.publisher
MDPI (Multidisciplinary Digital Publishing Institute)
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Reproducció digital del document publicat a: https://doi.org/10.3390/life12040537
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Life, 2022, vol. 12, núm. 4, p. 537
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Articles publicats (IdIBGi)
dc.rights
Attribution 4.0 International
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dc.subject
dc.title
Endothelial Dysfunction and Cardiovascular Risk in Obstructive Sleep Apnea: A Review Article
dc.type
info:eu-repo/semantics/article
dc.rights.accessRights
info:eu-repo/semantics/openAccess
dc.type.version
info:eu-repo/semantics/publishedVersion
dc.identifier.doi
dc.identifier.idgrec
035328
dc.type.peerreviewed
peer-reviewed
dc.identifier.eissn
2075-1729