Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor

The recent articles in Clin. Hemorheol. Microcirc. by Jung et al. [1–3], elegantly highlighted the thrombotic complications that arise in severe coronavirus disease 2019 (COVID-19) and discussed the role vascular injury and associated hyper inflammation play in bringing about multi-organ failure in...

Full description

Bibliographic Details
Main Author: Inal, Jameel
Format: Article
Language:English
Published: IOS Press 2020
Subjects:
Online Access:https://repository.londonmet.ac.uk/6084/1/ch_2020_75-4_ch-75-4-ch200958_ch-75-ch200958.pdf
_version_ 1804072563323699200
author Inal, Jameel
author_facet Inal, Jameel
author_sort Inal, Jameel
collection LMU
description The recent articles in Clin. Hemorheol. Microcirc. by Jung et al. [1–3], elegantly highlighted the thrombotic complications that arise in severe coronavirus disease 2019 (COVID-19) and discussed the role vascular injury and associated hyper inflammation play in bringing about multi-organ failure in severe disease. Coagulation and venous thromboembolism (VTE) in COVID-19 commonly presents as deep vein thrombosis (DVT) or pulmonary embolism (PE), and occurs because of inflammation, blood vessel injury and associated endothelial dysfunction. Likely contributors to this thrombotic milieu, hitherto little discussed in this COVID-19 pandemic, include Extracellular Vesicles (EVs), nanosized, cell-derived intercellular communicative vesicles, carrying proteins, bioactive lipids and miRNAs. Endothelial cell- (EC-) derived EVs (EEVs) are often released because of endothelial injury [4] and also likely to contribute to this prothrombotic environment. Whilst EVs and VTE in cancer has been much described, there is a significant knowledge gap concerning EVs and VTE in infectious disease. This letter considers how, as part of ongoing inflammation, complement may be activated in SARS-CoV-2 infection and so mediate EV biogenesis. It also assesses the role procoagulant EVs play in the context of coagulopathy and VTE in COVID-19, and their potential as a prognostic peripheral blood marker.
first_indexed 2024-07-09T04:01:08Z
format Article
id oai:repository.londonmet.ac.uk:6084
institution London Metropolitan University
language English
last_indexed 2024-07-09T04:01:08Z
publishDate 2020
publisher IOS Press
record_format eprints
spelling oai:repository.londonmet.ac.uk:60842020-10-09T11:54:25Z http://repository.londonmet.ac.uk/6084/ Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor Inal, Jameel 610 Medicine & health The recent articles in Clin. Hemorheol. Microcirc. by Jung et al. [1–3], elegantly highlighted the thrombotic complications that arise in severe coronavirus disease 2019 (COVID-19) and discussed the role vascular injury and associated hyper inflammation play in bringing about multi-organ failure in severe disease. Coagulation and venous thromboembolism (VTE) in COVID-19 commonly presents as deep vein thrombosis (DVT) or pulmonary embolism (PE), and occurs because of inflammation, blood vessel injury and associated endothelial dysfunction. Likely contributors to this thrombotic milieu, hitherto little discussed in this COVID-19 pandemic, include Extracellular Vesicles (EVs), nanosized, cell-derived intercellular communicative vesicles, carrying proteins, bioactive lipids and miRNAs. Endothelial cell- (EC-) derived EVs (EEVs) are often released because of endothelial injury [4] and also likely to contribute to this prothrombotic environment. Whilst EVs and VTE in cancer has been much described, there is a significant knowledge gap concerning EVs and VTE in infectious disease. This letter considers how, as part of ongoing inflammation, complement may be activated in SARS-CoV-2 infection and so mediate EV biogenesis. It also assesses the role procoagulant EVs play in the context of coagulopathy and VTE in COVID-19, and their potential as a prognostic peripheral blood marker. IOS Press 2020-09-25 Article PeerReviewed text en https://repository.londonmet.ac.uk/6084/1/ch_2020_75-4_ch-75-4-ch200958_ch-75-ch200958.pdf Inal, Jameel (2020) Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor. Clinical Hemorheology and Microcirculation, 75 (4). pp. 383-386. ISSN 1875-8622 10.3233/ch-200958
spellingShingle 610 Medicine & health
Inal, Jameel
Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title_full Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title_fullStr Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title_full_unstemmed Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title_short Complement-mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for COVID-19 in peripheral blood - letter to the Editor
title_sort complement mediated extracellular vesicle release as a measure of endothelial dysfunction and prognostic marker for covid 19 in peripheral blood letter to the editor
topic 610 Medicine & health
url https://repository.londonmet.ac.uk/6084/1/ch_2020_75-4_ch-75-4-ch200958_ch-75-ch200958.pdf
work_keys_str_mv AT inaljameel complementmediatedextracellularvesiclereleaseasameasureofendothelialdysfunctionandprognosticmarkerforcovid19inperipheralbloodlettertotheeditor