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Sleep Apnea Causes Endothelial Dysfunction. Find out how:

Endothelial Dysfunction and Cardiovascular Risk in Obstructive Sleep Apnea: A Review Article Miriam Peracaula 1, Daniela Torres 1, Paula Poyatos 1, Neus Luque 1, Eric Rojas 1, Anton Obrador 1, Ramon Orriols 1, Olga Tura-Ceide 1 2

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.

Keywords: cardiovascular disease; endothelial dysfunction; endothelial progenitor cells; obstructive sleep apnea; oxidative stress.


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