Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections

The bronchial vascular endothelial network plays important roles in pulmonary pathology during respiratory viral infections, including respiratory syncytial virus (RSV), influenza A(H1N1) and importantly SARS-Cov-2. All of these infections can be severe and even lethal in patients with underlying ri...

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Autores principales: Spiros Vlahopoulos, Ke Wang, Yaoyao Xue, Xu Zheng, Istvan Boldogh, Lang Pan
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/2bdac59a634b4eee861b8f1055178b5c
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spelling oai:doaj.org-article:2bdac59a634b4eee861b8f1055178b5c2021-11-25T17:11:05ZEndothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections10.3390/cells101130672073-4409https://doaj.org/article/2bdac59a634b4eee861b8f1055178b5c2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3067https://doaj.org/toc/2073-4409The bronchial vascular endothelial network plays important roles in pulmonary pathology during respiratory viral infections, including respiratory syncytial virus (RSV), influenza A(H1N1) and importantly SARS-Cov-2. All of these infections can be severe and even lethal in patients with underlying risk factors.A major obstacle in disease prevention is the lack of appropriate efficacious vaccine(s) due to continuous changes in the encoding capacity of the viral genome, exuberant responsiveness of the host immune system and lack of effective antiviral drugs. Current management of these severe respiratory viral infections is limited to supportive clinical care. The primary cause of morbidity and mortality is respiratory failure, partially due to endothelial pulmonary complications, including edema. The latter is induced by the loss of alveolar epithelium integrity and by pathological changes in the endothelial vascular network that regulates blood flow, blood fluidity, exchange of fluids, electrolytes, various macromolecules and responses to signals triggered by oxygenation, and controls trafficking of leukocyte immune cells. This overview outlines the latest understanding of the implications of pulmonary vascular endothelium involvement in respiratory distress syndrome secondary to viral infections. In addition, the roles of infection-induced cytokines, growth factors, and epigenetic reprogramming in endothelial permeability, as well as emerging treatment options to decrease disease burden, are discussed.Spiros VlahopoulosKe WangYaoyao XueXu ZhengIstvan BoldoghLang PanMDPI AGarticleendothelial cellsoxidative stresspulmonary edemarespiratory syncytial virusinfluenza H1N1SARS-Cov-2Biology (General)QH301-705.5ENCells, Vol 10, Iss 3067, p 3067 (2021)
institution DOAJ
collection DOAJ
language EN
topic endothelial cells
oxidative stress
pulmonary edema
respiratory syncytial virus
influenza H1N1
SARS-Cov-2
Biology (General)
QH301-705.5
spellingShingle endothelial cells
oxidative stress
pulmonary edema
respiratory syncytial virus
influenza H1N1
SARS-Cov-2
Biology (General)
QH301-705.5
Spiros Vlahopoulos
Ke Wang
Yaoyao Xue
Xu Zheng
Istvan Boldogh
Lang Pan
Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
description The bronchial vascular endothelial network plays important roles in pulmonary pathology during respiratory viral infections, including respiratory syncytial virus (RSV), influenza A(H1N1) and importantly SARS-Cov-2. All of these infections can be severe and even lethal in patients with underlying risk factors.A major obstacle in disease prevention is the lack of appropriate efficacious vaccine(s) due to continuous changes in the encoding capacity of the viral genome, exuberant responsiveness of the host immune system and lack of effective antiviral drugs. Current management of these severe respiratory viral infections is limited to supportive clinical care. The primary cause of morbidity and mortality is respiratory failure, partially due to endothelial pulmonary complications, including edema. The latter is induced by the loss of alveolar epithelium integrity and by pathological changes in the endothelial vascular network that regulates blood flow, blood fluidity, exchange of fluids, electrolytes, various macromolecules and responses to signals triggered by oxygenation, and controls trafficking of leukocyte immune cells. This overview outlines the latest understanding of the implications of pulmonary vascular endothelium involvement in respiratory distress syndrome secondary to viral infections. In addition, the roles of infection-induced cytokines, growth factors, and epigenetic reprogramming in endothelial permeability, as well as emerging treatment options to decrease disease burden, are discussed.
format article
author Spiros Vlahopoulos
Ke Wang
Yaoyao Xue
Xu Zheng
Istvan Boldogh
Lang Pan
author_facet Spiros Vlahopoulos
Ke Wang
Yaoyao Xue
Xu Zheng
Istvan Boldogh
Lang Pan
author_sort Spiros Vlahopoulos
title Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
title_short Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
title_full Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
title_fullStr Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
title_full_unstemmed Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections
title_sort endothelial dysfunction through oxidatively generated epigenetic mark in respiratory viral infections
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/2bdac59a634b4eee861b8f1055178b5c
work_keys_str_mv AT spirosvlahopoulos endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
AT kewang endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
AT yaoyaoxue endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
AT xuzheng endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
AT istvanboldogh endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
AT langpan endothelialdysfunctionthroughoxidativelygeneratedepigeneticmarkinrespiratoryviralinfections
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