Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses
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HYPERTENSION AND THE HEART (B UPADHYA, SECTION EDITOR)
Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses Eleni Gavriilaki 1 & Panagiota Anyfanti 1 & Maria Gavriilaki 2 & Antonios Lazaridis 1 & Stella Douma 1 & Eugenia Gkaliagkousi 1
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype Recent Findings Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Summary Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients. Keywords Thrombotic microangiopathy . COVID-19 . Complement . Endothelial dysfunction . Thrombosis . SARS-COV-2
Introduction Recent evidence suggests that signs and symptoms of severe coronavirus disease-2019 (COVID-19) infection resemble the clinical phenotype of endothelial dysfunction and share mutual pathophysiological mechanisms [1]. Importantly, endothelial dysfunction has been suggested as a main pathophysiological process in several viral infections, including previous coronaviruses [2, 3]. Experience from previous coronaviruses has triggered studies testing hypotheses on the role of the endothelial dysfunction in patients with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). As a result, recent
lines of evidence implicate endothelial dysfunction in the pathophysiology of this systemic infection. Endothelial dysfunction appears to be the common denominator of multiple clinical aspects of severe COVID-19 that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients. Therefore, we systematically reviewed current literature on the pathophysiology of endothelial dysfunction, evidence of endothelial dysfunction in coronaviruses, and particularly in COVID-19 focusing on the clinical phenotype.
Pathophysiology of Endothelial Dysfunction This article is part of the Topical Collection on Hypertension and the Heart * Eugenia Gkaliagkousi [email protected] 1
3rd Department of Internal Medicine, A
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