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Coronavirus disease (COVID-19) represents a public health crisis of global proportions. Caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), COVID-19 was first announced in December 2019 in Wuhan, the capital of China’s Hubei province. The symptoms most commonly reported by COVID-19 patients include cough, fever, and shortness of breath. Other major clinical events generally observed in COVID-19 patients include hypertension, thromboembolism, kidney disease, diabetes mellitus, cerebrovascular and neurologic disorders. These systemic manifestations strongly suggest that the virus is targeting the endothelium. The recent cases of Kawasaki-like “multisystem inflammatory syndrome” reported especially in young COVID-19 patients support our view of a fundamental role of the endothelium in the pathogenesis of COVID-19.


To access host cells, SARS-CoV-2 uses a surface glycoprotein known as spike; ACE2 has been shown to be a crucial co-receptor for coronavirus entry. Other receptors on the surface of human cells have been suggested to mediate the entry of SARS-CoV-2, including transmembrane serine protease 2 (TMPRSS2), sialic acid receptors, and extracellular matrix metalloproteinase inducer (CD147, also known as basigin). Additionally, cathepsin B and L have been shown to be critical entry factors in the pathogenesis of COVID-19. Intriguingly, all these factors involved in the entry of SARS-CoV-2 in the host cell are expressed by endothelial cells (Sardu et al. J. Clin. Med. 2020, 9(5), 1417; doi: 10.3390/jcm9051417).


In this meeting, we will discuss the most recent advances in the research exploring the mechanistic phenomena linking endothelial (dys)function to COVID-19 outcome.


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Fondazione Menarini
Fondazione Menarini, Centro Direzionale Milanofiori 20089 Rozzano (MI) - Edificio L - Strada 6
Tel. +39 02 55308110 Fax +39 02 55305739 C.F. 94265730484