Evidence map›Paper›PMID 28769795›Full record

ReviewFrontiers in pharmacology2017

Targeting TGF-β Mediated SMAD Signaling for the Prevention of Fibrosis.

Kelly L Walton, Katharine E Johnson, Craig A Harrison

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 332 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
332citing papers in PubMed, 3 pooled it
16.5field-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

332 citing papers in PubMed, 3 syntheses or guidelines pooled it, 554 citations in OpenAlex.

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  15. Molecular Engineering of the Helminth TGF-β Mimetics, TGM1 and TGM4, Reveals a Novel Antagonist of TGF-β Signaling in Fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  20. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review

272 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

3 authors at 1 institution in 1 country.

Kelly L WaltonGrowth Factor Therapeutics Laboratory, Department of Physiology, Monash University, ClaytonVIC, Australia.
Katharine E JohnsonGrowth Factor Therapeutics Laboratory, Department of Physiology, Monash University, ClaytonVIC, Australia.
Craig A HarrisonGrowth Factor Therapeutics Laboratory, Department of Physiology, Monash University, ClaytonVIC, Australia.
Monash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis occurs when there is an imbalance in extracellular matrix (ECM) deposition and degradation. Excessive ECM deposition results in scarring and thickening of the affected tissue, and interferes with tissue and organ homeostasis - mimicking an exaggerated "wound healing" response. Many transforming growth factor-β (TGF-β) ligands are potent drivers of ECM deposition, and additionally, have a natural affinity for the ECM, creating a concentrated pool of pro-fibrotic factors at the site of injury. Consequently, TGF-β ligands are upregulated in many human fibrotic conditions and, as such, are attractive targets for fibrosis therapy. Here, we will discuss the contribution of TGF-β proteins in the pathogenesis of fibrosis, and promising anti-fibrotic approaches that target TGF-β ligands.

Indexed as

activinfibrosismusclemyostatinpropeptideskeletalTGF-β

Identifiers

PMID28769795
PMCPMC5509761
OpenAlexW2735790845

What OpenQuestion 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 OpenQuestion graph.