COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

Article Article scientifique Revue de la littérature COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects eng 2021-06-28 2021-11 author Smadja David M. author Mentzer Steven J. author Fontenay Michaela author Laffan Mike A. author Ackermann Maximilian author Helms Julie author Jonigk Danny author Chocron Richard author Pier Gerald B. author Gendron Nicolas author Pons Stephanie author Diehl Jean-Luc author Margadant Coert author Guerin Coralie author Huijbers Elisabeth J. M. author Philippe Aurélien author Chapuis Nicolas 0000-0003-0601-3948 595948 author Nowak-Sliwinska Patrycja 848409 author Karagiannidis Christian author Sanchez Olivier author Kümpers Philipp author Skurnik David author Randi Anna M. author Griffioen Arjan W. 755-788 10.1007/s10456-021-09805-6 34184164 0969-6970 PMC8238037 https://link.springer.com/10.1007/s10456-021-09805-6 Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is presenting as a systemic disease associated with vascular inflammation and endothelial injury. Severe forms of SARS-CoV-2 infection induce acute respiratory distress syndrome (ARDS) and there is still an ongoing debate on whether COVID-19 ARDS and its perfusion defect differs from ARDS induced by other causes. Beside pro-inflammatory cytokines (such as interleukin-1 β [IL-1β] or IL-6), several main pathological phenomena have been seen because of endothelial cell (EC) dysfunction: hypercoagulation reflected by fibrin degradation products called D-dimers, micro- and macrothrombosis and pathological angiogenesis. Direct endothelial infection by SARS-CoV-2 is not likely to occur and ACE-2 expression by EC is a matter of debate. Indeed, endothelial damage reported in severely ill patients with COVID-19 could be more likely secondary to infection of neighboring cells and/or a consequence of inflammation. Endotheliopathy could give rise to hypercoagulation by alteration in the levels of different factors such as von Willebrand factor. Other than thrombotic events, pathological angiogenesis is among the recent findings. Overexpression of different proangiogenic factors such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) or placental growth factors (PlGF) have been found in plasma or lung biopsies of COVID-19 patients. Finally, SARS-CoV-2 infection induces an emergency myelopoiesis associated to deregulated immunity and mobilization of endothelial progenitor cells, leading to features of acquired hematological malignancies or cardiovascular disease, which are discussed in this review. Altogether, this review will try to elucidate the pathophysiology of thrombotic complications, pathological angiogenesis and EC dysfunction, allowing better insight in new targets and antithrombotic protocols to better address vascular system dysfunction. Since treating SARS-CoV-2 infection and its potential long-term effects involves targeting the vascular compartment and/or mobilization of immature immune cells, we propose to define COVID-19 and its complications as a systemic vascular acquired hemopathy. Dewey 615 European Research Council Optimized drug combinations for effective cancer treatment: a personalised approach ERC-680209 Swiss National Science Foundation Synergistic targeted drug combinations for induction of sensitivity to immune checkpoint inhibitors 310030–197878 31 Section des sciences pharmaceutiques 17 false 1325 Pharmacologie moléculaire Angiogenesis 24 4 34fb0d06-b2a9-43b6-94c1-efadbabad80e Article (Published version) Restricted Article-scientifique-from-crossref.pdf 1779694 application/pdf CC BY restrictedAccess Faculté des sciences / Section des sciences pharmaceutiques

Title	Published in	Access level	OA Policy	Year	Views	Downloads

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects	Angiogenesis			2021	160	1

Archive ouverte UNIGE

Chapuis, Nicolas