Evidence map›Paper›PMID 35306578›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022

Regulation of inflammation and apoptosis by GPR43 via JNK/ELK1 in acute lung injury.

Qiumin Xu, Jieying Xu, Yifan Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
    Review
  6. [Effects of nebulized selfZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Multiple Beneficial Effects of Aloesone fromMolecules (Basel, Switzerland) · 2023
    Article
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

3 authors at 1 institution in 1 country.

Qiumin Xu *Emergency Department, School of Medicine, Nanjing Tongren HospitalSoutheast UniversityJiangning District, Longhu Wenxin garden, No. 99, Lantai street, Nanjing, 211102, Jiangsu, China.
Jieying Xu *Special Functions Section, The Fourth Sanatorium Area of Hangzhou Special Service Sanatorium Center of Air Force, Nanjing, 210000, Jiangsu, China.
Yifan WuEmergency Department, School of Medicine, Nanjing Tongren HospitalSoutheast UniversityJiangning District, Longhu Wenxin garden, No. 99, Lantai street, Nanjing, 211102, Jiangsu, China. wuyifanyf21@163.com.ORCID http://orcid.org/0000-0002-1039-5048
Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is mostly relevant to acute and severe lung inflammation. We first utilized lipopolysaccharide (LPS) to induce mice for establishing a mouse model of ALI and detected decreased expression of GPR43 in the lung tissue in mice with ALI. Mice expressing increased GPR43 showed improvement in lung injury compared to LPS-treated mice. Additionally, ALI mice transfected with lenti-GPR43 significantly decreased the mRNA levels of TNF-α, IL-1β, IL-6, MPO, COX2 and iNOS, and apoptosis levels in the lungs, as well as the phosphorylation levels of JNK and ELK1 compared to LPS-treated mice with lenti-vector infection. Subsequently, we employed LPS to induce alveolar type ii epithelial cells and observed that Ov-GPR43 infection markedly reduced the expression levels of inflammatory factors and apoptosis levels, while exposure of cells to anisomycin was also effective in blunting the effects of Ov-GPR43 on these processes. Taken together, these results demonstrate a role of GPR43 in mediating lung injury through JNK/ELK1 and imply the therapeutic potential of targeting GPR43 against ALI.

Indexed as

Acute Lung InjuryLipopolysaccharidesAnimalsApoptosisInflammationLungMiceLipopolysaccharidesAcute lung injuryELK1GPR43InflammationJNK

Identifiers

PMID35306578
OpenAlexW4220674443

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.