Evidence map›Paper›PMID 34748205›Full record

ReviewMolecular neurobiology2022

Neutrophil Extracellular Traps Exacerbate Ischemic Brain Damage.

Congqin Li, Ying Xing, Yuqian Zhang, Yan Hua, Jian Hu, Yulong Bai

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 3 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026
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19 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

6 authors at 1 institution in 1 country.

Congqin LiDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China.
Ying XingDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China.
Yuqian ZhangDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China.
Yan HuaDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China.
Jian HuDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China.
Yulong BaiDepartment of Rehabilitation Medicine, Huashan Hospital, Fudan University, No. 12 Middle Wulumuqi Road, Jing'an District, Shanghai, 200040, China. dr_baiyl@fudan.edu.cn.ORCID http://orcid.org/0000-0003-0461-1506
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most acute strokes are ischemic, and subsequent neuroinflammation promotes further damage leading to cell death but also plays a beneficial role by promoting cellular repair. Neutrophils are forerunners to brain lesions after ischemic stroke and exert elaborate functions. While neutrophil extracellular traps (NETs) possess a fundamental antimicrobial function within the innate immune system under physiological circumstances, increasing evidence indicates that NETosis, the release process of NETs, occurs in the pathogenic process of stroke. In this review, we focus on the processes of NET formation and clearance, the temporal and spatial alterations of neutrophils and NETs after ischemic damage, and how NETs are involved in several stroke-related phenomena. Generally, NET formation and release processes depend on the generation of reactive oxygen species (ROS) and the activation of nuclear peptidylarginine deiminase-4 (PAD4). The acid-base environment, oxygen concentration, and iron ions around the infarct may also impact NET formation. DNase 1 has been identified as the primary degrader of NETs in serum, while reactive microglia are expected to inhibit the formation of NETs around ischemic lesions by phagocytosis of neutrophils. The neutrophils and NETs are present in the perivascular space ipsilateral to the infarct arising after ischemic damage, peaking between 1 and 3 days postischemia, but their location in the brain parenchyma remains controversial. After the ischemic injury, NETs are involved in the destruction of neurological function primarily by disrupting the blood-brain barrier and promoting thrombosis. The potential effects of NETs on various ischemic nerve cells need to be further investigated, especially in the chronic ischemic phase.

Indexed as

AnimalsBrainExtracellular TrapsHumansInflammationIschemic StrokeNeutrophilsReactive Oxygen SpeciesReactive Oxygen SpeciesInflammationIschemic strokeNeural immuneNeutrophil extracellular trapsNeutrophilsPAD4

Identifiers

PMID34748205
OpenAlexW3214074266

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.