Evidence map›Paper›PMID 35309344›Full record

ReviewFrontiers in immunology2022

NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond.

Yuanfeng Zhu, Xiaoli Chen, Xin Liu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
14.1field-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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.

  1. Pooled it
  2. SARS-CoV-2 Immune Complex-Mediated Neutrophil Activation.Open forum infectious diseases · 2025
    Trial
  3. Article
  4. Article
  5. Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  16. COVID-19 and Lung Cancer Interactions: A Literature Review.Medical sciences (Basel, Switzerland) · 2025
    Review
  17. COVID-19 Infection, Drugs, and Liver Injury.Journal of clinical medicine · 2025
    Review
  18. Article
  19. Review
  20. Review

49 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 1 institution in 1 country.

Yuanfeng ZhuClinical Medical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, China.
Xiaoli ChenClinical Medical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, China.
Xin LiuClinical Medical Research Center, Southwest Hospital, Army Military Medical University, Chongqing, China.
Southwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with SARS-CoV-2, the causative agent of the Coronavirus disease 2019 (COVID-19) pandemic, causes respiratory problems and multifaceted organ dysfunction. A crucial mechanism of COVID-19 immunopathy is the recruitment and activation of neutrophils at the infection site, which also predicts disease severity and poor outcomes. The release of neutrophil extracellular traps (NETs), occurring during a regulated form of neutrophil cell death known as NETosis, is a key effector function that mediates harmful effects caused by neutrophils. Abundant NETosis and NET generation have been observed in the neutrophils of many COVID-19 patients, leading to unfavorable coagulopathy and immunothrombosis. Moreover, excessive NETosis and NET generation are now more widely recognized as mediators of additional pathophysiological abnormalities following SARS-CoV-2 infection. In this minireview, we introduce subtypes of NET-producing neutrophils (e.g., low-density granulocytes) and explain the biological importance of NETs and the protein cargos of NETs in COVID-19. In addition, we discuss the mechanisms by which SARS-CoV-2 causes NETosis by upregulating viral processes (e.g., viral entry and replication) as well as host pro-NET mechanisms (e.g., proinflammatory mediator release, platelet activation, and autoantibody production). Furthermore, we provide an update of the main findings of NETosis and NETs in immunothrombosis and other COVID-19-related disorders, such as aberrant immunity, neurological disorders, and post COVID-19 syndromes including lung fibrosis, neurological disorder, tumor progression, and deteriorated chronic illness. Finally, we address potential prospective COVID-19 treatment strategies that target dysregulated NETosis and NET formation

Indexed as

AnimalsApoptosisBlood Coagulation DisordersCarcinogenesisCOVID-19Extracellular TrapsFibrosisHumansLungNeutrophilsSARS-CoV-2ThromboinflammationCOVID-19immunopathologyimmunothrombosisNETosisNETspost COVID-19 syndrome

Identifiers

PMID35309344
PMCPMC8924116
OpenAlexW4214914468

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.