Vascular dysfunction in COVID-19 patients: update on SARS-CoV-2 infection of endothelial cells and the role of long non-coding RNAs. Issue 21 (11th November 2022)

• Record Type: Journal Article
• Authors: Pelisek, Jaroslav; Reutersberg, Benedikt; Greber, Urs F; Zimmermann, Alexander
• Is Part Of: Clinical science. Volume 136:Issue 21(2022)
• Page Start: 1571
• Page End: 1590
• Publication Date: 2022-11-11
• Subjects: cardiovascular disorder (CVD) -- COVID-19 -- endothelial cells (ECs) -- ong non-coding RNA -- SARS-CoV-2 -- smooth muscle cells (SMCs); Medicine -- Periodicals; Biochemistry -- Periodicals; 616
• DOI: 10.1042/CS20220235
• Languages: English
• ISSNs: 0143-5221

Abstract

Abstract: Although COVID-19 is primarily a respiratory disease, it may affect also the cardiovascular system. COVID-19 patients with cardiovascular disorder (CVD) develop a more severe disease course with a significantly higher mortality rate than non-CVD patients. A common denominator of CVD is the dysfunction of endothelial cells (ECs), increased vascular permeability, endothelial-to-mesenchymal transition, coagulation, and inflammation. It has been assumed that clinical complications in COVID-19 patients suffering from CVD are caused by SARS-CoV-2 infection of ECs through the angiotensin-converting enzyme 2 (ACE2) receptor and the cellular transmembrane protease serine 2 (TMPRSS2) and the consequent dysfunction of the infected vascular cells. Meanwhile, other factors associated with SARS-CoV-2 entry into the host cells have been described, including disintegrin and metalloproteinase domain-containing protein 17 (ADAM17), the C-type lectin CD209L or heparan sulfate proteoglycans (HSPG). Here, we discuss the current data about the putative entry of SARS-CoV-2 into endothelial and smooth muscle cells. Furthermore, we highlight the potential role of long non-coding RNAs (lncRNAs) affecting vascular permeability in CVD, a process that might exacerbate disease in COVID-19 patients.