Evidence map›Paper›PMID 28208683›Full record

ArticleInternational journal of molecular sciences2017

Plasma Gelsolin Induced Glomerular Fibrosis via the TGF-β1/Smads Signal Transduction Pathway in IgA Nephropathy.

Lei Zhang, Changsong Han, Fei Ye, Yan He, Yinji Jin, Tianzhen Wang, Yiqi Wu, Yang Jiang, Fengmin Zhang, Xiaoming Jin

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Combined Inhibition of the TGF-β1/Smad Pathway byInternational journal of molecular sciences · 2023
    Article
  4. Article
  5. Review
  6. Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Antioxidant and Wound Healing Property of Gelsolin in 3T3-L1 Cells.Oxidative medicine and cellular longevity · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. 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

10 authors.

Lei ZhangDepartment of Pathology, Harbin Medical University, Harbin 150081, China. Zhangleiyy12@126.com.
Changsong HanDepartment of Pathology, Harbin Medical University, Harbin 150081, China. han050122@163.com.
Fei YeDepartment of Pathology, Harbin Medical University, Harbin 150081, China. yefeiboer@163.com.
Yan HeDepartment of Pathology, Harbin Medical University, Harbin 150081, China. he_yan419@163.com.
Yinji JinDepartment of Pathology, Harbin Medical University, Harbin 150081, China. jinyinji66@126.com.
Tianzhen WangDepartment of Pathology, Harbin Medical University, Harbin 150081, China. wtzpath@163.com.
Yiqi WuDepartment of Pathology, Harbin Medical University, Harbin 150081, China. wuyiqidd@126.com.
Yang JiangDepartment of Pathology, Harbin Medical University, Harbin 150081, China. jiangyang1978@hotmail.com.
Fengmin ZhangDepartment of Microbiology, Harbin Medical University, Harbin 150081, China. fengminzhang@ems.hrbmu.edu.cn.
Xiaoming JinDepartment of Pathology, Harbin Medical University, Harbin 150081, China. jinxm5554@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glomerular fibrosis has been shown to be closely related to the progression and prognosis of IgA nephropathy (IgAN). However, mechanism underlying IgAN glomerular fibrosis remains unclear. Recently, our study showed that plasma gelsolin (pGSN) was decreased in the serum of an IgAN mouse model and that pGSN deposition was found in the glomeruli. Another cytokine, TGF-β1, which is closely related to glomerular fibrosis, was also found to be highly expressed in the glomeruli. In the present study, we report that pGSN induces glomerular fibrosis through the TGF-β1/Smads signal transduction pathway. This is supported by the following findings: human mesangial cells (HMCs) show remarkable morphological changes and proliferation in response to co-stimulation with pGSN and polymeric IgA1 (pIgA1) from IgAN patients compared to other controls. Moreover, ELISA assays showed that more TGF-β1 secretion was found in HMCs supernatants in the co-stimulation group. Further experiments showed increased TGF-β1, Smad3, p-Smad2/3, Smad4, and collagen 1 and decreased Smad7 expression in the co-stimulation group. Our present study implied that the synergistic effect of pGSN and pIgA induced glomerular fibrosis via the TGF-β1/Smads signal transduction pathway. This might be a potential mechanism for the glomerular fibrosis observed in IgAN patients.

Indexed as

Signal TransductionBiomarkersCase-Control StudiesCell ProliferationFibrosisFluorescent Antibody TechniqueGelsolinGlomerulonephritis, IGAHumansMesangial CellsSmad ProteinsTransforming Growth Factor beta1BiomarkersGelsolinSmad ProteinsTransforming Growth Factor beta1glomerular fibrosisIgA nephropathyplasma gelsolinTGF-β1/Smadssignal transduction pathway

Identifiers

PMID28208683
PMCPMC5343925

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Registered trials

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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.