Evidence map›Paper›PMID 34116654›Full record

ReviewJournal of biomedical science2021

C-type lectins and extracellular vesicles in virus-induced NETosis.

Pei-Shan Sung, Shie-Liang Hsieh

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Neutrophil Extracellular Traps in Viral Infections.Pathogens (Basel, Switzerland) · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. An Updated Review of Potential Drug Targets for Japanese Encephalitis.Central nervous system agents in medicinal chemistry · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024
    Review
  12. Extracellular Vesicles: The Invisible Heroes and Villains of COVID-19 Central Neuropathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. The role of cell death in SARS-CoV-2 infection.Signal transduction and targeted therapy · 2023
    Review
  18. Article
  19. Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Pei-Shan SungGenomics Research Center, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan.
Shie-Liang HsiehGenomics Research Center, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan. slhsieh@gate.sinica.edu.tw.ORCID http://orcid.org/0000-0001-9415-346X
Genomics Research Center, Academia Sinica · TWNational Yang Ming Chiao Tung University · TW

Funding

Academia Sinica 106-2101-01-11-01, 107-2101-01-18-03, AS-IA-109-L02Academia Sinica AS-IA-109-L02Ministry of Science and Technology, Taiwan 106-2321-B-001-037, MOST 106-2320-B-001-023-MY3
6 · The paper itself

Abstract

Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Furthermore, excessive NET formation (NETosis) is associated with disease severity in patients suffering from SARS-CoV-2-induced multiple organ injuries. Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and other members of C-type lectin family (L-SIGN, LSECtin, CLEC10A) have been reported to interact with viral glycans to facilitate virus spreading and exacerbates inflammatory reactions. Moreover, spleen tyrosine kinase (Syk)-coupled C-type lectin member 5A (CLEC5A) has been shown as the pattern recognition receptor for members of flaviviruses, and is responsible for DV-induced cytokine storm and Japanese encephalomyelitis virus (JEV)-induced neuronal inflammation. Moreover, DV activates platelets via CLEC2 to release extracellular vesicles (EVs), including microvesicles (MVs) and exosomes (EXOs). The DV-activated EXOs (DV-EXOs) and MVs (DV-MVs) stimulate CLEC5A and Toll-like receptor 2 (TLR2), respectively, to enhance NET formation and inflammatory reactions. Thus, EVs from virus-activated platelets (PLT-EVs) are potent endogenous danger signals, and blockade of C-type lectins is a promising strategy to attenuate virus-induced NETosis and intravascular coagulopathy.

Indexed as

Blood PlateletsCOVID-19Cytokine Release SyndromeEncephalitis, JapaneseEncephalitis Virus, JapaneseExtracellular TrapsHumansLectins, C-TypePlatelet ActivationSARS-CoV-2Signal TransductionLectins, C-TypeCLEC2CLEC5ACOVID-19C-type lectin receptor (CLR)Dengue virus (DV)Exosome (EXO)Extracellular vesicle (EV)Microvesicle (MV)PlateletSARS-CoV-2TLR

Identifiers

PMID34116654
PMCPMC8193014
OpenAlexW3167557254

What OpenQuestion 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 OpenQuestion graph.