Evidence map›Paper›PMID 22009442›Full record

ArticleInflammation2012

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) mediates p38 mitogen-activated protein kinase activation and signal transduction in peripheral blood mononuclear cells from patients with lupus nephritis.

Liu Zhi-Chun, Zhou Qiao-Ling, Liu Zhi-Qin, Li Xiao-Zhao, Zuo Xiao-xia, Tang Rong

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. TWEAK and the progression of renal disease: clinical translation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2014
    Review
  12. Article
  13. The TWEAK-Fn14 system as a potential drug target.British journal of pharmacology · 2013
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. 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

6 authors at 3 institutions in 1 country.

Liu Zhi-ChunDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of Suzhou University, Suzhou, China.
Zhou Qiao-Ling
Liu Zhi-Qin
Li Xiao-Zhao
Zuo Xiao-xia
Tang Rong
Xiangya Hospital Central South University · CNCentral South University · CNHebei University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forty-two patients with systemic lupus erythematosus (SLE), including 26 patients with renal damage and 16 without, and 20 healthy controls were included in the study. The isolated peripheral blood mononuclear cells (PBMCs) were treated with a p38 inhibitor (SB203580) or anti-tumor necrosis factor-like weak inducer of apoptosis (TWEAK) mAb, with or without phytohemagglutinin/phorbol myristate acetate (PHA/PMA) stimulation. Western blot experiments were used to evaluate the protein expression of TWEAK and p38 MAPK in PBMCs .Next, the contents of interleukin-10 (IL-10) and monocyte chemoattractant protein-1 (MCP-1) in the supernatant were measured by ELISA. The results showed that expression of TWEAK protein in PBMCs from lupus nephritis patients was significantly higher than that from SLE patients without renal damage and healthy controls. PHA/PMA simulation could upregulate the productions of TWEAK and p-p38MAPK in PBMCs from patients with SLE. Anti-TWEAK mAb treatment downregulated both TWEAK and p-p38 MAPK expression in PBMCs, as well as IL-10 and MCP-1 in the supernatant; SB203580 had the same effect on cytokine production in PBMC, but had no effect on the expression of TWEAK. Our results suggested that TWEAK-p38 MAPK-IL-10, MCP-1 signaling pathway in PBMC played an important pathogenic role in lupus nephritis.

Indexed as

AdolescentAdultAntibodies, MonoclonalCells, CulturedChemokine CCL2FemaleHumansImidazolesInterleukin-10Leukocytes, MononuclearLupus Erythematosus, SystemicLupus NephritisMaleMAP Kinase Signaling SystemMiddle Agedp38 Mitogen-Activated Protein KinasesAntibodies, MonoclonalCCL2 protein, humanChemokine CCL2ImidazolesInterleukin-10p38 Mitogen-Activated Protein KinasesPhytohemagglutininsPyridinesReceptors, Tumor Necrosis FactorSB 203580Tetradecanoylphorbol AcetateTumor Necrosis FactorsTWEAK Receptor

Identifiers

PMID22009442
OpenAlexW1987478743

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.