Evidence map›Paper›PMID 17003485›Full record

ArticleThe American journal of pathology2006

ERK, p38, and Smad signaling pathways differentially regulate transforming growth factor-beta1 autoinduction in proximal tubular epithelial cells.

Mei Zhang, Donald Fraser, Aled Phillips

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Regulation and Signaling of TGF-β Autoinduction.International journal of molecular and cellular medicine · 2021
    Review
  9. Article
  10. Article
  11. RIPK3: A New Player in Renal Fibrosis.Frontiers in cell and developmental biology · 2020
    Review
  12. [Mechanism of p38 mitogen activated protein kinase signaling pathway on promoting the hypertrophy of human lumbar ligamentum flavum via transforming growth factor βZhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Genetic deletion of cell division autoantigen 1 retards diabetes-associated renal injury.Journal of the American Society of Nephrology : JASN · 2013
    Article
  20. 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.

Mei ZhangInstitute of Nephrology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN UK. phillipsao@cf.ac.uk.
Donald Fraser
Aled Phillips
Cardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-beta1 is a mediator of the final common pathway of fibrosis associated with progressive renal disease, a process in which proximal tubular cells (PTCs) are known to play an important part. The aim of the current study was to examine the mechanism of PTC TGF-beta1 autoinduction. The addition of TGF-beta1 led to increased amounts of TGF-beta1 mRNA and increased de novo protein synthesis. The addition of TGF-beta1 led to increased phosphorylation of R-Smads and activation of extracellular signal-regulated kinase mitogen-activated protein (MAP) kinase and p38 MAP kinase pathways. Use of a dominant-negative Smad3 (Smad3 DN) expression vector, Smad3 small interfering RNA, and inhibition of extracellular signal-regulated kinase and p38 MAP kinase pathways with the chemical inhibitors PD98059 or SB203580 suggested that activation of these signaling pathways occurred independently. Smad3 DN expression, Smad3 small interfering RNA, or the addition of PD98059 inhibited TGF-beta1-dependent stimulation of TGF-beta1 mRNA. Furthermore, Smad3 blockade specifically inhibited activation of the transcription factor AP-1 by TGF-beta1, whereas PD98059 prevented TGF-beta1-dependent nuclear factor-kappaB activation. In contrast inhibition of p38 MAP kinase inhibited de novo TGF-beta1 protein synthesis but did not influence TGF-beta1 mRNA expression or activation of either transcription factor. In summary, in PTCs, TGF-beta1 autoinduction requires the coordinated action of independently regulated Smad and non-Smad pathways. Furthermore these pathways regulate distinct transcriptional and translational components of TGF-beta1 synthesis.

Indexed as

Transcriptional ActivationCells, CulturedEpithelial CellsExtracellular Signal-Regulated MAP KinasesFlavonoidsHumansImidazolesKidney Tubules, Proximalp38 Mitogen-Activated Protein KinasesPolyribosomesProtein BiosynthesisProtein Kinase InhibitorsPyridinesRNA, MessengerSignal TransductionSmad3 Protein2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneExtracellular Signal-Regulated MAP KinasesFlavonoidsImidazolesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsPyridinesRNA, MessengerSB 203580Smad3 ProteinSMAD3 protein, humanTransforming Growth Factor beta1

Identifiers

PMID17003485
PMCPMC1698849
OpenAlexW2092988724

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.