Evidence map›Paper›PMID 25901787›Full record

ArticleInternational journal of molecular medicine2015

CCN5 attenuates profibrotic phenotypes of fibroblasts through the Smad6-CCN2 pathway: Potential role in epidural fibrosis.

Honghai Xu, Cong Liu, Zhengming Sun, Xiong Guo, Yuelin Zhang, Mengting Liu, Peng Li

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2015. 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
0.8field-weighted citation impact, top 28% 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, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. CCN5/WISP2 and metabolic diseases.Journal of cell communication and signaling · 2018
    Review
  11. 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

7 authors at 3 institutions in 1 country.

Honghai XuDepartment of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Cong LiuXi'an Medical College, Xi'an, Shaanxi 710061, P.R. China.
Zhengming SunDepartment of Orthopaedics, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Xiong GuoDepartment of Public Health, Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Yuelin ZhangDepartment of Neurosurgery, The Third Affiliated Hospital (Shaanxi Provincial People's Hospital), Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Mengting LiuXi'an Medical College, Xi'an, Shaanxi 710061, P.R. China.
Peng LiXi'an Medical College, Xi'an, Shaanxi 710061, P.R. China.
Shaanxi Provincial People's Hospital · CNXi'an Medical University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidural fibrosis is characterized by the development of dense and thick scar tissue adjacent to the dural mater and ranked as the major contributor for post-operative pain recurrence after laminectomy or discectomy. Recently, CCN5 exhibited an inhibitory effect on connective tissue growth factor (CTGF)/CCN2 (a critical regulator for fibrotic disease)‑mediated fibrogenesis. However, its function in epidural fibrosis and the underlying mechanisms involved remain to be determined. In this study, an obvious downregulation of CCN5 was observed in scar tissues from laminectomized rats, concomitant with a marked upregulation of CCN2, suggesting a potential negative regulatory role of CCN5 in fibrogenesis. Furthermore, CCN5 overexpression notably mitigated transforming growth factor‑β1-enhanced fibroblast viability and proliferation. Of note, CCN5 upregulation inhibited the switch of fibroblasts into myofibroblasts as its overexpression abrogated the expression of the myofibroblast marker, α-smooth muscle actin (α-SMA). CCN5 upregulation also reduced an increase in collagen type I, α1 (COL1A1) and total collagen concentrations. Additionally, CCN5 over-expression decreased CCN2 expression and increased Smad6 phosphorylation. Mechanism analysis revealed that blocking Smad6 signaling significantly ameliorated the inhibitory effect of CCN5 on the CCN2 levels, accompanied by the reduction in cell proliferation and collagen production. These results confirm that CCN5 exerts an anti-fibrotic function by regulating the Smad6-CCN2 pathway, thereby indicating a potential approach for ameliorating epidural fibrosis after laminectomy.

Indexed as

ActinsAnimalsCCN Intercellular Signaling ProteinsCell ProliferationCells, CulturedCollagen Type ICollagen Type I, alpha 1 ChainConnective Tissue Growth FactorFibroblastsFibrosisLaminectomyMalePhosphorylationRatsRats, Inbred LewRepressor ProteinsActa2 protein, ratActinsCCN2 protein, ratCCN5 protein, ratCCN Intercellular Signaling ProteinsCollagen Type ICollagen Type I, alpha 1 ChainConnective Tissue Growth FactorRepressor ProteinsRNA, Small InterferingSmad6 ProteinSmad6 protein, ratTransforming Growth Factor beta1

Identifiers

PMID25901787
PMCPMC4494601
OpenAlexW2074800468

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.