Evidence map›Paper›PMID 36000086›Full record

ReviewMedComm2022

Molecular mechanisms and therapeutic target of NETosis in diseases.

Jiayu Huang, Weiqi Hong, Meihua Wan, Limin Zheng

Open access · goldAbstract readReview
In one paragraph

Review in MedComm, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 2 pooled it
14.6field-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

150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 187 citations in OpenAlex.

  1. Pooled it
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  17. Gut · 2026
    Article
  18. Review
  19. NETosis mediates tick blood pool formation.The Journal of veterinary medical science · 2026
    Article
  20. Article

90 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

4 authors at 2 institutions in 2 countries.

Jiayu HuangLaboratory of Aging Research and Cancer Drug Target State Key Laboratory of Biotherapy National Clinical Research Center for Geriatrics West China Hospital Sichuan University Chengdu China.
Weiqi HongLaboratory of Aging Research and Cancer Drug Target State Key Laboratory of Biotherapy National Clinical Research Center for Geriatrics West China Hospital Sichuan University Chengdu China.ORCID https://orcid.org/0000-0003-1668-2301
Meihua WanDepartment of Integrated Traditional Chinese and Western Medicine West China Hospital Sichuan University Chengdu Sichuan China.
Limin ZhengGuangdong Province Key Laboratory of Pharmaceutical Functional Genes MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou China.
Sichuan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence shows that neutrophils can protect the host against pathogens in multiple ways, including the formation and release of neutrophil extracellular traps (NETs). NETs are web-like structures composed of fibers, DNA, histones, and various neutrophil granule proteins. NETs can capture and kill pathogens, including bacteria, viruses, fungi, and protozoa. The process of NET formation is called NETosis. According to whether they depend on nicotinamide adenine dinucleotide phosphate (NADPH), NETosis can be divided into two categories: "suicidal" NETosis and "vital" NETosis. However, NET components, including neutrophil elastase, myeloperoxidase, and cell-free DNA, cause a proinflammatory response and potentially severe diseases. Compelling evidence indicates a link between NETs and the pathogenesis of a number of diseases, including sepsis, systemic lupus erythematosus, rheumatoid arthritis, small-vessel vasculitis, inflammatory bowel disease, cancer, COVID-19, and others. Therefore, targeting the process and products of NETosis is critical for treating diseases linked with NETosis. Researchers have discovered that several NET inhibitors, such as toll-like receptor inhibitors and reactive oxygen species scavengers, can prevent uncontrolled NET development. This review summarizes the mechanism of NETosis, the receptors associated with NETosis, the pathology of NETosis-induced diseases, and NETosis-targeted therapy.

Indexed as

NET inhibitionNETosisneutrophilneutrophil extracellular trap

Identifiers

PMID36000086
PMCPMC9390875
OpenAlexW4293275525

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.