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Editorial
. 2020 Jul 30;56(1):2001634.
doi: 10.1183/13993003.01634-2020. Print 2020 Jul.

Endothelial cell dysfunction: a major player in SARS-CoV-2 infection (COVID-19)?

Alice Huertas  1   2   3 , David Montani  4   2   3 , Laurent Savale  4   2   3 , Jérémie Pichon  4   2   3 , Ly Tu  4   2 , Florence Parent  4   2   3 , Christophe Guignabert  4   2 , Marc Humbert  4   2   3
Affiliations
Editorial

Endothelial cell dysfunction: a major player in SARS-CoV-2 infection (COVID-19)?

Alice Huertas et al. Eur Respir J. .

Abstract

Endothelial cell dysfunction and impaired microcirculatory function contribute markedly to life-threatening complications of COVID-19, such as venous thromboembolic disease and multiple organ involvement https://bit.ly/3cZMjKV

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Conflict of interest statement

Conflict of interest: A. Huertas has nothing to disclose. Conflict of interest: D. Montani reports grants and personal fees from Actelion and Bayer, personal fees from GSK, Pfizer, Chiesi and Boehringer, grants, personal fees and non-financial support from MSD, non-financial support from Acceleron, outside the submitted work. Conflict of interest: L. Savale reports personal fees and non-financial support from Actelion and Bayer, grants and personal fees from GSK, outside the submitted work. Conflict of interest: J. Pichon has nothing to disclose. Conflict of interest: L. Tu has nothing to disclose. Conflict of interest: F. Parent reports grants from Bayer, CSL Behring and Sanofi, outside the submitted work. Conflict of interest: C. Guignabert has nothing to disclose. Conflict of interest: M. Humbert reports grants and personal fees from Actelion, Bayer, GSK and Acceleron, personal fees from Merck and United Therapeutics, outside the submitted work.

Figures

FIGURE 1
FIGURE 1
Schematic representation of hypothetical mechanisms by which the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes endothelial dysfunction and pulmonary vascular changes. Following cleavage of its S protein, SARS-CoV-2 was reported to enter human cells via binding to angiotensin-converting enzyme 2 (ACE-2). This transmembrane ACE-2 receptor is widely expressed in various pulmonary cells including type II alveolar cells, macrophages, endothelial, smooth muscle cells and perivascular pericytes. This causes uncontrolled inflammation (1), accompanied by micro-thrombosis and occlusion of small pulmonary vessels (2), and impaired endothelial regulation of vascular tone (3), leading to alveolo-capillary barrier disruption (4). Ang: angiotensin; AT: angiotensin receptor; IL: interleukin; MAS: macrophage activation syndrome; MIF: macrophage migration inhibitory factor; NO: nitric oxide; PAF: platelet activating factor; PAI-1: plasminogen activator inhibitor-1; PGI2: prostaglandin I2; TF: tissue factor; TNF: tumour necrosis factor; tPA: tissue plasminogen activator.
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