Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Endothelial Dysfunction in SARS CoV-2 Infection

Version 1 : Received: 12 February 2022 / Approved: 15 February 2022 / Online: 15 February 2022 (11:05:22 CET)

A peer-reviewed article of this Preprint also exists.

Nappi, F.; Avtaar Singh, S.S. Endothelial Dysfunction in SARS-CoV-2 Infection. Biomedicines 2022, 10, 654. Nappi, F.; Avtaar Singh, S.S. Endothelial Dysfunction in SARS-CoV-2 Infection. Biomedicines 2022, 10, 654.

Journal reference: Biomedicines 2022, 10, 654
DOI: 10.3390/biomedicines10030654

Abstract

One of the hallmarks of the SARS-CoV-2 infection has been the inflammatory process that played a role in its pathogenesis, resulting in mortality within susceptible individuals. This uncontrolled inflammatory process leads to severe systemic symptoms via multiple pathways, however, the role of endothelial dysfunction and thrombosis have not been truly explored. This review aims to highlight the pathogenic mechanisms of these inflammatory triggers leading to thrombogenic complications. There are direct and indirect pathogenic pathways of the infection that are examined in detail. We also describe the case of carotid artery thrombosis in a patient following the SARS-CoV-2 infection, while reviewing the literature on the role of ACE2, the endothelium, and the different mechanisms by which SARS-CoV-2 may manifest both acutely and chronically. We also highlight differences from the other coronaviruses that have made this infection pandemic with similarities to the influenza virus.

Keywords

endothelial dysfunction; SARS-CoV-2 infection; thrombosis, angiotensin-converting enzyme-2; angiogenesis

Subject

MEDICINE & PHARMACOLOGY, Cardiology

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