Evidence map›Paper›PMID 27010330›Full record

ArticlePloS one2016

Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-β1/Smad Signaling Pathway.

Lirong Liu, Yuanyuan Wang, Rui Yan, Shuang Li, Mingjun Shi, Ying Xiao, Bing Guo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Smad3 Signatures in Renal Inflammation and Fibrosis.International journal of biological sciences · 2022
    Review
  10. Article
  11. [Oxymatrine improves renal fibrosis and inflammation in diabetic rats by modulating CHK1/2 phosphorylation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  12. Article
  13. Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 1 institution in 1 country.

Lirong LiuDepartment of Clinical Hematology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Yuanyuan WangDepartment of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, China.
Rui YanDepartment of Nephrology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Shuang LiDepartment of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, China.
Mingjun ShiDepartment of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, China.
Ying XiaoDepartment of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, China.
Bing GuoDepartment of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, China.
Guiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β1 (TGF-β1) signaling has been shown to play a critical role in the development of diabetic nephropathy (DN). The nuclear transcription co-repressor Ski-related novel protein N (SnoN) is an important negative regulator of TGF-β1/Smad signal transduction, and subsequent biological responses including tubule epithelial-mesenchymal transition (EMT), extracellular matrix accumulation and tubulointerstitial fibrosis. Oxymatrine (OM) is an alkaloid extracted from the Chinese herb Sophora japonica and has been demonstrated to prevent fibrosis. However, the anti-fibrosis effect of OM in DN is still unclear. In this study, we cultured normal rat renal tubular epithelial cells (NRK52Es) in high glucose and high glucose plus OM, and detected the expression of E-cadherin, α-SMA, FN, TGF-β1, SnoN, Arkadia, p-Smad2 and p-Smad3 and poly-ubiquitination of SnoN. The results showed that E-cadherin and SnoN expression in NRK52Es decreased significantly, but poly-ubiquitination of SnoN, TGF-β1, α-SMA, FN, Arkadia, p-Smad2 and p-Smad3 expression significantly increased due to high glucose stimulation, which could be almost completely reversed by OM, suggesting that OM may alleviate EMT induced by high glucose via upregulating SnoN expression and inhibiting TGF-β1/Smad signaling pathway activation. Hence, OM could be a novel therapeutic for DN.

Indexed as

AlkaloidsAnimalsCell LineEpithelial-Mesenchymal TransitionFibronectinsGene Expression RegulationGlucoseKidney TubulesMatrinesNerve Tissue ProteinsQuinolizinesRatsSignal TransductionSmad ProteinsSophoraTranscription FactorsAlkaloidsFibronectinsGlucoseMatrinesNerve Tissue ProteinsoxymatrineQuinolizinesRnf111 protein, ratSkil_v1 protein, ratSmad ProteinsTranscription FactorsTransforming Growth Factor beta1Ubiquitin-Protein Ligases

Identifiers

PMID27010330
PMCPMC4807015
OpenAlexW2304275581

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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.