SARS-CoV-2, the cause of COVID-19, has generated a global emergency. The endothelium is a target of SARS-CoV-2, generating endothelial dysfunction, an essential step for the development of cardiovascular complications. The number of endothelial progenitor cells acts as an indicator of vascular damage. However, its role in SARS-CoV-2 is unknown. The aim of this study was to quantify the number of endothelial colony forming cells (ECFCs) and assess for the first time if there is a significant increase after SARS-CoV-2 infection. This study also evaluates whether the number of ECFC is related to the presence of pulmonary embolism (PE), and if this increase correlates with any of the clinical parameters studied. A total of 63 subjects were recruited including 32 subjects 3-months after overcoming COVID-19 and 31 healthy controls. The results confirm the presence of vascular sequelae in post-COVID-19 patients, with an abnormal increase in the number of ECFCs in blood circulation compared to controls (2,81±2,33 vs 1,23±1,86, p=0.001). There was no difference in ECFC production in COVID-19 who presented acute PE compared to those that did not (3,21±2,49 vs 2,50±2,23, p>0.05). The appearance of ECFC colonies in COVID-19 patients was significantly related to male gender (p=0.003), the presence of systemic hypertension (p=0.01) and elevated hemoglobin levels (p=0.02) at the time of ECFC isolation and lower PaO 2 levels (p=0.01) at admission. Whether these results indicate a prompt response of the patient to repair the damaged endothelium or reflect a post-infection injury that will persist in time is not known.

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.

Pulmonary hypertension (PH) is a progressive disease characterized by elevated artery pressures and pulmonary vascular resistance. Underlying mechanisms comprise endothelial dysfunction, pulmonary artery remodeling and vasoconstriction. Several studies have shown evidence of the critical role of oxidative stress in PH pathophysiology. Alteration of redox homeostasis produces excessive generation of reactive oxygen species, inducing oxidative stress and the subsequent alteration of biological molecules. Exacerbations in oxidative stress production can lead to alterations in nitric oxide signaling pathways, contributing to the proliferation of pulmonary arterial endothelial cells and smooth muscle cells, inducing PH development. Recently, antioxidant therapy has been suggested as a novel therapeutic strategy for PH pathology. However, the favorable outcomes observed in preclinical studies have not been consistently reproduced in clinical practice. Therefore, targeting oxidative stress as a therapeutic intervention for PH is an area that is still being explored. This review summarizes the contribution of oxidative stress to the pathogenesis of the different types of PH and suggests antioxidant therapy as a promising strategy for PH treatment.