Evidence map›Paper›PMID 34164484›Full record

ArticleAnnals of translational medicine2021

Lipopolysaccharide-induced inflammation in human peritoneal mesothelial cells is controlled by ERK1/2-CDK5-PPARγ axis.

Zukai Li, Junxia Feng, Shen Yang, Ping Meng, Jingchun Li, Hongyan Li, Xuejuan Gao, Yunfang Zhang

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Exosomal PPARγ derived from macrophages suppresses LPS-induced peritonitis by negative regulation of CD14/TLR4 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

8 authors at 3 institutions in 1 country.

Zukai LiThe Third School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Junxia FengThe Central Laboratory, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Shen YangDepartment of Nephrology, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Ping MengThe Central Laboratory, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Jingchun LiThe Central Laboratory, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Hongyan LiDepartment of Nephrology, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Xuejuan GaoKey Laboratory of Functional Protein Research of Guangdong Higher Education Institutes and MOE Key Laboratory of Tumor Molecular Biology, Institute of Life and Health Engineering, Jinan University, Guangzhou, China.
Yunfang ZhangDepartment of Nephrology, Affiliated Huadu Hospital, Southern Medical University (People's Hospital of Huadu District), Guangzhou, China.
Southern Medical University · CNJinan University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPeritonitis is a common complication in which the peritoneum becomes inflamed. Peroxisome proliferator-activated receptor (PPAR)γ agonists and extracellular signal-regulated kinases 1/2 (ERK1/2) inactivation have been found to restore damage caused by lipopolysaccharide-induced (LPS) inflammation. This study aimed to investigate the association between PPARγ and ERK1/2 in LPS-induced inflammation in peritonitis.

methodsHuman peritoneal mesothelial cells were maintained in Dulbecco's Modified Eagle Medium and treated with LPS under a series of different concentrations and treatment times. Cellular interleukins-1βeta (IL-1β), cellular interleukins-6 (IL-6), cellular interleukins-12 (IL-12) were measured by enzyme-linked immunosorbent assay (ELISA) assay. Expression or activation of cyclin-dependent kinase (CDK)5, ERK1/2, and PPARγ was detected using quantitative real-time PCR and/or western blot.

resultsLPS induced dose- and time-dependent increments in the cellular IL-1β, IL-6, and IL-12 contents, cyclin-dependent kinase 5 (CDK5) expression, and PPARγ

conclusionsOur results suggested that LPS-induced inflammation in human peritoneal mesothelial cells can be partly suppressed by inhibiting the ERK1/2/CDK5/PPARγ axis.

Indexed as

cyclin-dependent kinase 5 (CDK5)Extracellular signal-regulated kinases 1/2 (ERK1/2)lipopolysaccharide (LPS)peritonitisperoxisome proliferator-activated receptor γ (PPARγ)

Identifiers

PMID34164484
PMCPMC8184493
OpenAlexW3164534374

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.