Potential value of circulating endothelial cells for the diagnosis and treatment of COVID-19

Abstract

The ongoing severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic has been a formidable global challenge. As yet, there are very few drugs to treat this infection and no vaccine is currently available. It has gradually become apparant that coronavirus disease 2019 (COVID-19) is not a simple disease involving a single organ; rather, many vital organs and systems are affected. The endothelium is one target of SARS-CoV-2. Damaged endothelial cells, which break away from organs and enter the bloodstream to form circulating endothelial cells, were recently reported as putative biomarkers for COVID-19. Modulation of the expression level of sphingosine-1 phosphate via sphingosine kinase activation can control endothelial cell proliferation and apoptosis. As such, it may be possible to obtain a sensitive and specific diagnosis of the severity of COVID-19 by assessing the absolute number and the viable/apoptotic ratio of circulating endothelial cells. Furthermore, a focus on the endothelium could help to develop a strategy for COVID-19 treatment from the perspective of endothelial protection and repair.

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

“…It has been increasingly appreciated that COVID-19 is not only an infectious disease involving the lung; but also, a vascular disease affecting extrapulmonary organs [ 174 ]. Endothelial dysfunction-induced endotheliitis/endothelialitis/endotheliopathy following SARS-CoV-2 infection arises from a plethora of physiopathological mechanisms, including both direct mechanism of virus infection or indirect mechanisms such as paracrine effects of infected cells [ 2 , 68 ].…”

Influencia de la obesidad en la severidad de la infección por SARS-CoV-2

“…Encontraron células endoteliales infectadas con SARS-CoV-2 e inflamación endotelial difusa, lo que sugiere que los receptores de angiotensina II se encuentran altamente distribuidos en las células endoteliales de múltiples órganos. La infección por este virus provoca daño endotelial extenso relacionado con la apoptosis, que finalmente conduce a la inducción (50) de endotelitis en varios órganos . Por eso se cree que los fármacos antiinflamatorios anticitocinas, los inhibidores de la enzima convertidora de la angiotensina (IECA) y las estatinas pueden representar (51) estrategias relevantes para el manejo de COVID-19 , en particular para los pacientes más vulnerables y con peor pronóstico, como aquellos con disfunción endotelial preexistente asociada con sexo masculino, enfermedades respiratorias crónicas, hipertensión arterial, diabetes mellitus 2 y (39) obesidad .…”

A hitchhiker's guide through the COVID-19 galaxy

“…Blood samples of COVID-19 patients show significantly higher levels of circulating endothelial cells (CECs) on admission than those with other respiratory infections, demonstrating early and extensive endothelial injury [12]. Epithelial and endothelial damage may begin long before a patient is admitted to the ICU, and CECs, if available, may be of prognostic value now [167]. Other markers of endothelial activation with discriminatory value at this stage are von Willebrand Factor (vWF), angiopoietin (Angpt-1/Angpt-2 ratio, see below) and soluble urokinase plasminogen activator receptor (suPAR).…”