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Verfasst von:Schönrich, Günther [VerfasserIn]   i
 Raftery, Martin J. [VerfasserIn]   i
 Samstag, Yvonne [VerfasserIn]   i
Titel:Devilishly radical NETwork in COVID-19
Titelzusatz:Oxidative stress, neutrophil extracellular traps (NETs), and T cell suppression
Verf.angabe:Günther Schönrich, Martin J. Raftery, Yvonne Samstag
E-Jahr:2020
Jahr:4 July 2020
Umfang:18 S.
Teil:volume:77
 year:2020
 elocationid:100741
 pages:1-18
 extent:18
Fussnoten:Gesehen am 25.06.2021
Titel Quelle:Enthalten in: Advances in Biological Regulation
Ort Quelle:New York, NY [u.a.] : Elsevier, 2012
Jahr Quelle:2020
Band/Heft Quelle:77(2020), Artikel-ID 100741, Seite 1-18
ISSN Quelle:2212-4934
Abstract:Pandemic coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and poses an unprecedented challenge to healthcare systems due to the lack of a vaccine and specific treatment options. Accordingly, there is an urgent need to understand precisely the pathogenic mechanisms underlying this multifaceted disease. There is increasing evidence that the immune system reacts insufficiently to SARS-CoV-2 and thus contributes to organ damage and to lethality. In this review, we suggest that the overwhelming production of reactive oxygen species (ROS) resulting in oxidative stress is a major cause of local or systemic tissue damage that leads to severe COVID-19. It increases the formation of neutrophil extracellular traps (NETs) and suppresses the adaptive arm of the immune system, i.e. T cells that are necessary to kill virus-infected cells. This creates a vicious cycle that prevents a specific immune response against SARS-CoV-2. The key role of oxidative stress in the pathogenesis of severe COVID-19 implies that therapeutic counterbalancing of ROS by antioxidants such as vitamin C or NAC and/or by antagonizing ROS production by cells of the mononuclear phagocyte system (MPS) and neutrophil granulocytes and/or by blocking of TNF-α can prevent COVID-19 from becoming severe. Controlled clinical trials and preclinical models of COVID-19 are needed to evaluate this hypothesis.
DOI:doi:10.1016/j.jbior.2020.100741
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://dx.doi.org/10.1016/j.jbior.2020.100741
 Volltext: https://www.sciencedirect.com/science/article/pii/S221249262030052X?via%3Dihub
 DOI: https://doi.org/10.1016/j.jbior.2020.100741
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Acetylcysteine
 Antioxidants
 Ascorbic Acid
 Betacoronavirus
 Coronavirus Infections
 COVID-19
 Cytokines
 Extracellular Traps
 Host-Pathogen Interactions
 Humans
 Immune system
 Immunity, Innate
 Lymphopenia
 Neutrophil extracellular traps (NETs)
 Neutrophils
 NF-kappa B
 Oxidative stress
 Oxidative Stress
 Pandemics
 Pneumonia, Viral
 Reactive Oxygen Species
 SARS-CoV-2
 T cells
 T-Lymphocytes
K10plus-PPN:176125135X
Verknüpfungen:→ Zeitschrift

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