Evidence map›Paper›PMID 41956858›Full record

ReviewTrends in cell biology2026

Eosinophil extracellular traps: heterogeneity of their stimuli, components, and functions.

Jingdai Zhang, Xiaohang Liu, Guo-Ping Shi, Wei Chen, Shuyang Zhang

Abstract readReview
In one paragraph

Review in Trends in cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

5 authors.

Jingdai ZhangDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100006, China.
Xiaohang LiuDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100006, China; Department of Internal Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100006, China.
Guo-Ping ShiZhongda Hospital, Advanced Institute for Life and Health, School of Medicine, Southeast University, Nanjing 210096, China; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Electronic address: gpshi@seu.edu.cn.
Wei ChenDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100006, China. Electronic address: chenwei6@medmail.com.cn.
Shuyang ZhangDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100006, China; State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Beijing, China. Electronic address: shuyangzhang103@nrdrs.org.

Funding

Role of Mast cells in Alzheimer's DiseaseR01AG063839 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2020 to 2024
$3.1M
Role of group 2 innate lymphoid cells in myocardial infarctionR01HL157073 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2022 to 2025
$2.7M
Role of ILC2 and eosinophils in abdominal aortic aneurysmR01HL151627 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2021 to 2024
$2.7M
Role of eosinophil cationic proteins in cardiac hypertrophyR01HL166538 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2023 to 2025
$2.1M
Role of CLCA1 as a MIF decoy inhibitor in abdominal aortic aneurysmsR01HL170000 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter Libby · 2024 to 2026
$2.1M
NHLBI NIH HHS R01 HL151627NHLBI NIH HHS R01 HL157073NHLBI NIH HHS R01 HL166538NHLBI NIH HHS R01 HL170000NIA NIH HHS R01 AG063839
6 · The paper itself

Abstract

Eosinophils participate in immune regulation through their granule proteins and cytokines. Recent studies demonstrate eosinophil functional versatility through the mechanism of eosinophil extracellular traps (EETs). EET formation occurs via suicidal eosinophil extracellular trap cell death (EETosis) and vital EET release. EETs contain chromatin- or mitochondrial-derived DNA, granule proteins, nuclear proteins, and cytosolic components that vary depending on the type and intensity of stimuli. Synthetic compounds, pathogenic microorganisms, endogenous molecules, and co-stimulatory factors stimulate EET formation via diverse signaling pathways through receptors that rely on or operate independently of NADPH oxidase-mediated reactive oxygen species production and peptidylarginine deiminase-4-dependent histone modification. Necroptosis, pyroptosis, and autophagy pathways also contribute to EET biogenesis and subset heterogeneity. Here, we summarize EET formation, compositional profile, and functional heterogeneity across disease states, as well as the future potential for novel immune intervention.

Indexed as

EosinophilsExtracellular TrapsAnimalsHumansReactive Oxygen SpeciesSignal TransductionReactive Oxygen Specieschromatin DNAeosinophileosinophil extracellular trapmitochondrial DNA

Identifiers

PMID41956858
PMCPMC13078697

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Registered trials

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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.