Evidence map›Paper›PMID 26257392›Full record

ArticleJournal of cellular and molecular medicine2015

Salvianolic acid B-induced microRNA-152 inhibits liver fibrosis by attenuating DNMT1-mediated Patched1 methylation.

Fujun Yu, Zhongqiu Lu, Bicheng Chen, Xiaoli Wu, Peihong Dong, Jianjian Zheng

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. An EED/PRC2-H19 Loop Regulates Cerebellar Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Frontiers in pharmacology · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Frontiers in pharmacology · 2022
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Fujun YuDepartment of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhongqiu LuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Bicheng ChenKey Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xiaoli WuDepartment of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Peihong DongDepartment of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Jianjian ZhengKey Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) was reported to be involved in the activation of hepatic stellate cells (HSCs), contributing to the development of liver fibrosis. Epithelial-mesenchymal transition can be promoted by the Hedgehog (Hh) pathway. Patched1 (PTCH1), a negative regulatory factor of the Hh signalling pathway, was down-regulated during liver fibrosis and associated with its hypermethylation status. MicroRNAs (miRNAs) are reported to play a critical role in the control of various HSCs functions. However, miRNA-mediated epigenetic regulations in EMT during liver fibrosis are seldom studied. In this study, Salvianolic acid B (Sal B) suppressed the activation of HSCs in CCl4 -treated mice and mouse primary HSCs, leading to inhibition of cell proliferation, type I collagen and alpha-smooth muscle actin. We demonstrated that the antifibrotic effects caused by Sal B were, at least in part, via inhibition of EMT and the Hh pathway. In particular, up-regulation of PTCH1 was associated with decreased DNA methylation level after Sal B treatment. Accordingly, DNA methyltransferase 1 (DNMT1) was attenuated by Sal B in vivo and in vitro. The knockdown of DNMT1 in Sal B-treated HSCs enhanced PTCH1 expression and its demethylation level. Interestingly, increased miR-152 in Sal B-treated cells was responsible for the hypomethylation of PTCH1 by Sal B. As confirmed by the luciferase activity assay, DNMT1 was a direct target of miR-152. Further studies showed that the miR-152 inhibitor reversed Sal B-mediated PTCH1 up-regulation and DNMT1 down-regulation. Collectively, miR-152 induced by Sal B, contributed to DNMT1 down-regulation and epigenetically regulated PTCH1, resulting in the inhibition of EMT in liver fibrosis.

Indexed as

AnimalsBenzofuransDepsidesEpigenesis, GeneticLiver CirrhosisMethylationMiceMicroRNAsPatched-1 ReceptorRepressor ProteinsBenzofuransDepsidesDmap1 protein, mouseMicroRNAsMIRN152 microRNA, mousePatched-1 ReceptorPtch1 protein, mouseRepressor Proteinssalvianolic acid BDNA methylationDNA methyltransferasehepatic stellate cellsmicroRNA-152Patched1

Identifiers

PMID26257392
PMCPMC4627567
OpenAlexW1730166774

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.