Evidence map›Paper›PMID 26747705›Full record

ReviewThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2016

TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis.

Fengyun Xu, Changwei Liu, Dandan Zhou, Lei Zhang

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05637216 (A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients), which is not on this map. Cited by 412 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
412citing papers in PubMed, 1 pooled it
26.3field-weighted citation impact, top 1% 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.

NCT05637216 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients

TypeinterventionalSponsorShaw Cancer CenterRan2023 to 2027Enrolled43ConditionsRadiation Induced FibrosisArmsLosartan 25 milligram capsule, Placebo
3 · Its place in the literature

Who cites it

412 citing papers in PubMed, 1 synthesis or guideline pooled it, 711 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Dendrobium officinale Polysaccharides Protected against CClChinese journal of integrative medicine · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

352 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Fengyun XuSchool of Pharmacy (FX, DZ, LZ)
Changwei LiuAnhui Medical University, Hefei 230022, ChinaDepartment of Pharmacy, The First Affiliated Hospital of Anhui Medical University (CL)
Dandan ZhouSchool of Pharmacy (FX, DZ, LZ)
Lei ZhangSchool of Pharmacy (FX, DZ, LZ)
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-beta1 (TGF-β1), a key member in the TGF-β superfamily, plays a critical role in the development of hepatic fibrosis. Its expression is consistently elevated in affected organs, which correlates with increased extracellular matrix deposition. SMAD proteins have been studied extensively as pivotal intracellular effectors of TGF-β1, acting as transcription factors. In the context of hepatic fibrosis, SMAD3 and SMAD4 are pro-fibrotic, whereas SMAD2 and SMAD7 are protective. Deletion of SMAD3 inhibits type I collagen expression and blocks epithelial-myofibroblast transition. In contrast, disruption of SMAD2 upregulates type I collagen expression. SMAD4 plays an essential role in fibrosis disease by enhancing SMAD3 responsive promoter activity, whereas SMAD7 negatively mediates SMAD3-induced fibrogenesis. Accumulating evidence suggests that divergent miRNAs participate in the liver fibrotic process, which partially regulates members of the TGF-β/SMAD signaling pathway. In this review, we focus on the TGF-β/SMAD and other relative signaling pathways, and discussed the role and molecular mechanisms of TGF-β/SMAD in the pathogenesis of hepatic fibrosis. Moreover, we address the possibility of novel therapeutic approaches to hepatic fibrosis by targeting to TGF-β/SMAD signaling.

Indexed as

Signal TransductionHumansLiver CirrhosisSmad ProteinsTransforming Growth Factor betaSmad ProteinsTransforming Growth Factor betaEpithelial-myofibroblast transitionhepatic fibrosismiRNAsTGF-β/SMAD

Identifiers

PMID26747705
PMCPMC4810800
OpenAlexW2256103742

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.