Evidence map›Paper›PMID 32773102›Full record

ReviewAdvances in biological regulation2020

Devilishly radical NETwork in COVID-19: Oxidative stress, neutrophil extracellular traps (NETs), and T cell suppression.

Günther Schönrich, Martin J Raftery, Yvonne Samstag

Open access · hybridAbstract readReview
In one paragraph

Review in Advances in biological regulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 5 pooled it
15.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

139 citing papers in PubMed, 5 syntheses or guidelines pooled it, 227 citations in OpenAlex.

  1. Pooled it
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  11. Unraveling NETs in Sepsis: From Cellular Mechanisms to Clinical Relevance.International journal of molecular sciences · 2025
    Review
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  16. Observational
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79 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Günther SchönrichInstitute of Virology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Berlin, Germany. Electronic address: guenther.schoenrich@charite.de.
Martin J RafteryInstitute of Virology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Berlin, Germany.
Yvonne SamstagSection Molecular Immunology, Institute of Immunology, Heidelberg University Hospital, Heidelberg, Germany. Electronic address: yvonne.samstag@urz.uni-heidelberg.de.
Humboldt-Universität zu Berlin · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

PandemicsAcetylcysteineAntioxidantsAscorbic AcidBetacoronavirusCoronavirus InfectionsCOVID-19CytokinesExtracellular TrapsHost-Pathogen InteractionsHumansImmunity, InnateLymphopeniaNeutrophilsNF-kappa BOxidative StressAcetylcysteineAntioxidantsAscorbic AcidCytokinesNF-kappa BReactive Oxygen SpeciesCOVID-19Immune systemLymphopeniaNeutrophil extracellular traps (NETs)Oxidative stressT cells

Identifiers

PMID32773102
PMCPMC7334659
OpenAlexW3039378699

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.