Evidence map›Paper›PMID 36423907›Full record

ArticleThe European respiratory journal2023

Eosinophils protect against pulmonary hypertension through 14-HDHA and 17-HDHA.

Ting Shu, Jiawei Zhang, Yitian Zhou, Zhihua Chen, Jinqiu Li, Qihao Tang, Wenqi Lei, Yanjiang Xing, Jing Wang, Chen Wang

Open access · hybridAbstract read
In one paragraph

Article in The European respiratory journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Docosahexaenoic acid supplementation inhibits monocyte exhaustion memory formation during sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. RareInnovation (Cambridge (Mass.)) · 2026
    Article
  7. Article
  8. Docosahexaenoic Acid and Its Metabolites Protect against Ozone-induced Pulmonary Inflammation.American journal of respiratory cell and molecular biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Observational
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  14. Article
  15. Article
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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

10 authors at 2 institutions in 1 country.

Ting ShuState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0001-5837-2593
Jiawei ZhangState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0003-4253-9015
Yitian ZhouState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-9543-5386
Zhihua ChenKey Laboratory of Respiratory Disease of Zhejiang Province, Dept of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jinqiu LiState Key Laboratory of Medical Molecular Biology, Dept of Physiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Qihao TangState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Wenqi LeiState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yanjiang XingState Key Laboratory of Medical Molecular Biology, Dept of Physiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.ORCID 0000-0003-3108-5599
Jing WangState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China wangjing@ibms.pumc.edu.cn.ORCID 0000-0003-2410-5408
Chen WangState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Dept of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary hypertension (PH) is a life-threatening disease featuring pulmonary vessel remodelling and perivascular inflammation. The effect, if any, of eosinophils (EOS) on the development of PH remains unclear.

methodsEOS infiltration and chemotaxis were investigated in peripheral blood and lung tissues from pulmonary arterial hypertension (PAH) patients without allergic history and from sugen/hypoxia-induced PH mice. The role of EOS deficiency in PH development was investigated using

resultsThere was a lower percentage of EOS in peripheral blood but higher infiltration in lung tissues from PAH patients and PH mice. PAH/PH lungs showed increased EOS-related chemokine expression, mainly C-C motif chemokine ligand 11 derived from adventitial fibroblasts. EOS deficiency aggravated PH in rodents, accompanied by increased neutrophil and monocyte/macrophage infiltration. EOS highly expressed arachidonate 15-lipoxygenase (ALOX15). 14-hydroxy docosahexaenoic acid (14-HDHA) and 17-HDHA were critical downstream oxylipins produced by EOS, which showed anti-inflammatory effects on recruitment of neutrophils and monocytes/macrophages through N-formyl peptide receptor 2. They also repressed pulmonary artery smooth muscle cell (PASMC) proliferation by activating peroxisome proliferator-activated receptor γ and blunting Stat3 phosphorylation.

conclusionsIn PH development without external stimuli, peripheral blood exhibits a low EOS level. EOS play a protective role by suppressing perivascular inflammation and maintaining PASMC homeostasis

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionAnimalsCell ProliferationCells, CulturedEosinophilsFamilial Primary Pulmonary HypertensionHypoxiaInflammationMiceMice, KnockoutMyocytes, Smooth MusclePulmonary ArteryRatsTandem Mass Spectrometry

Identifiers

PMID36423907
PMCPMC9978164
OpenAlexW4309924770

What OpenQuestion holds

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LicenceCC BY-NC
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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.