Evidence map›Paper›PMID 31718044›Full record

ReviewCells2019

TGF-β in Hepatic Stellate Cell Activation and Liver Fibrogenesis-Updated 2019.

Bedair Dewidar, Christoph Meyer, Steven Dooley, And Nadja Meindl-Beinker

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 490 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
490citing papers in PubMed, 2 pooled it
42.2field-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.

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

490 citing papers in PubMed, 2 syntheses or guidelines pooled it, 752 citations in OpenAlex.

  1. Pooled it
  2. [Meta-analysis of the efficacy of the Fuzheng Huayu formula in the treatment of hepatitis B-associated liver fibrosis or cirrhosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024
    Pooled it
  3. Trial
  4. Review
  5. Article
  6. 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
  7. Article
  8. Article
  9. Article
  10. Review
  11. [Alcohol liver disease: immunoregulatory mechanisms and precision therapeutic targets].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026
    Review
  18. Article
  19. Review
  20. Article

430 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 3 institutions in 2 countries.

Bedair DewidarDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Christoph MeyerDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
Steven DooleyDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
And Nadja Meindl-BeinkerDepartment of Medicine II, Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany.
University Hospital Heidelberg · DEHeidelberg University · DETanta University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is an advanced liver disease condition, which could progress to cirrhosis and hepatocellular carcinoma. To date, there is no direct approved antifibrotic therapy, and current treatment is mainly the removal of the causative factor. Transforming growth factor (TGF)-β is a master profibrogenic cytokine and a promising target to treat fibrosis. However, TGF-β has broad biological functions and its inhibition induces non-desirable side effects, which override therapeutic benefits. Therefore, understanding the pleiotropic effects of TGF-β and its upstream and downstream regulatory mechanisms will help to design better TGF-β based therapeutics. Here, we summarize recent discoveries and milestones on the TGF-β signaling pathway related to liver fibrosis and hepatic stellate cell (HSC) activation, emphasizing research of the last five years. This comprises impact of TGF-β on liver fibrogenesis related biological processes, such as senescence, metabolism, reactive oxygen species generation, epigenetics, circadian rhythm, epithelial mesenchymal transition, and endothelial-mesenchymal transition. We also describe the influence of the microenvironment on the response of HSC to TGF-β. Finally, we discuss new approaches to target the TGF-β pathway, name current clinical trials, and explain promises and drawbacks that deserve to be adequately addressed.

Indexed as

Disease SusceptibilityAnimalsAutophagyBiomarkersCellular MicroenvironmentCellular SenescenceCircadian RhythmEnergy MetabolismEpigenesis, GeneticGene Expression RegulationHepatic Stellate CellsHumansLiver CirrhosisMyofibroblastsOxidative StressSignal TransductionBiomarkersTransforming Growth Factor betahepatic stellate cellsliver fibrosismyofibroblastsTGF-β

Identifiers

PMID31718044
PMCPMC6912224
OpenAlexW2986691533

What Socratic 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 Socratic graph.