COVID-19 and Endothelial Dysfunction: Biomarkers and Potential Drug Mechanisms

Abstract

Since the fi rst report of pneumonia outbreak in Wuhan by the end of 2019, Coronavirus Disease 2019 (COVID-19) has become a global pandemic; causing millions of deaths globally and aff ecting the rest of worldwide population. The disease is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which enters hosts by inhabiting Angiotensin-Converting Enzyme-2 (ACE-2) receptors expressed in the endothelium layer of not only the respiratory tracts, but also various organs in the body. COVID-19 has been reported to trigger multiple cardiovascular manifestations. Since endothelial dysfunction plays an important role in cardiovascular events and the endothelium is heavily involved in COVID-19 pathophysiology, it is important to investigate their associations and previously established drug potencies to improve endothelial functions as possible treatment options for COVID-19. In this review, we summarize endothelial dysfunction biomarkers involved in COVID-19 and drugs that have shown potential endothelial protective properties to better understand the incidence of endothelial dysfunction in COVID-19 and its future treatment. We searched in PubMed, Wiley Online Library, EBSCO, ScienceDirect databases for literatures containing following keywords: “Endothelial dysfunction”, “COVID-19”, and “biomarkers”. Eligible publications were then assessed and studied to comprise our literature review. A total of 96 studies matched our criteria and provided scientifi c evidences for our review. Materials were then compiled into a review summarizing endothelial biomarkers involved in COVID-19 and potentially repurposed drugs targeting endothelium for COVID-19.Various endothelial dysfunction biomarkers were found to be elevated in COVID19 and is found to be related to its severity, such as adhesion molecules, selectins, PAI-1, and von Willebrand Factors. Multiple drugs targeting the endothelium are also potential and some are under investigation for COVID-19.

Profiles of Plasminogen Activator Inhibitor-1 Levels in Healthcare Workers with Latent Tuberculosis and Non-Latent Tuberculosis Infections (Healthy Control)

“…These cytokines trigger endothelial cell activation and promote the release of t-PA and PAI-1. Activated endothelial cells express increased levels of PAI-1, inhibit t-PA and u-PA, and trigger a shift in the hemostatic balance to a procoagulant state [18].…”