COVID-19: the vasculature unleashed

Laure-Anne Teuwen, Vincent Geldhof, Alessandra Pasut, Peter Carmeliet, Laure-Anne Teuwen, Vincent Geldhof, Alessandra Pasut, Peter Carmeliet

Abstract

On the basis of emerging evidence from patients with COVID-19, we postulate that endothelial cells are essential contributors to the initiation and propagation of severe COVID-19. Here, we discuss current insights into the link between endothelial cells, viral infection and inflammatory changes and propose novel therapeutic strategies.

Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1. Proposed vessel–lung tissue interface in…
Fig. 1. Proposed vessel–lung tissue interface in normal state and in COVID-19 disease.
a | On the left, the normal interface between the alveolar space and endothelial cells is depicted; the right side highlights pathophysiological features of coronavirus disease 2019 (COVID-19) in the lung, including loss of vascular integrity (1), activation of the coagulation pathway (2) and inflammation (3). b–d | Proposed contributing endothelial cell-specific mechanisms are detailed. ROS, reactive oxygen species; S1PR1, sphingosine 1 phosphate receptor 1; VWF, von Willebrand factor.

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Source: PubMed

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