Evidence map›Paper›PMID 39147414›Full record

ArticleThe European respiratory journal2024

LPG 18:0 is a general biomarker of asthma and inhibits the differentiation and function of regulatory T-cells.

Abudureyimujiang Aili, Yuqing Wang, Ying Shang, Lijiao Zhang, Huan Liu, Zemin Li, Lixiang Xue, Yahong Chen, Yongchang Sun, Xu Zhang and 2 more

Abstract read
In one paragraph

Article in The European respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Metabolomic and immunological signatures of asthma severity in children.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Abudureyimujiang AiliDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Yuqing WangCenter of Basic Medical Research, Institute of Medical Innovation and Research, Peking University Third Hospital, Beijing, China.
Ying ShangDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Lijiao ZhangDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Huan LiuDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Zemin LiDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Lixiang XueCenter of Basic Medical Research, Institute of Medical Innovation and Research, Peking University Third Hospital, Beijing, China.
Yahong ChenDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Yongchang SunDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
Xu ZhangTianjin Key Laboratory of Metabolic Diseases, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Center for Cardiovascular Diseases, Research Center of Basic Medical Sciences, Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
Rong JinDepartment of Immunology, School of Basic Medical Sciences, Peking University, NHC Key Laboratory of Medical Immunology (Peking University), Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Beijing, China.
Chun ChangDepartment of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China doudou_1977@vip.163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe diagnosis, severity assessment, and development of therapeutic strategies for asthma are crucial aspects of disease management. Since biomarkers are reliable tools in disease management, we aimed to identify and explore asthma-associated biomarkers and investigate their mechanisms.

methodsLipidomics was used to profile serum glycerophospholipids in asthmatic patients and controls. The absolute concentration of lysophosphatidylglycerol (LPG) 18:0 was quantified in various asthma subtypes. Mouse asthma models were used to confirm its potential as a biomarker and investigate its mechanisms

resultsThe serum glycerophospholipid profile varied between asthmatic patients and control group, with LPG 18:0 levels being notably higher in asthmatic patients, correlating with asthma severity and control level.

conclusionsThis study identifies that serum levels of LPG 18:0 are generally elevated in asthmatics and serve as a biomarker for asthma. LPG 18:0 impairs Treg function

Indexed as

AsthmaBiomarkersCell DifferentiationT-Lymphocytes, RegulatoryAdultAnimalsApoptosisCase-Control StudiesCell ProliferationDisease Models, AnimalFemaleHumansLipidomicsLysophospholipidsMaleMiceBiomarkersLysophospholipidsReactive Oxygen Species

Identifiers

PMID39147414
PMCPMC11618814

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.