Evidence map›Paper›PMID 28432134›Full record

ReviewCold Spring Harbor perspectives in biology2018

TGF-β1 Signaling and Tissue Fibrosis.

Kevin K Kim, Dean Sheppard, Harold A Chapman

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2018. 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 448 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
448citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

448 citing papers in PubMed, 2 syntheses or guidelines pooled it, 747 citations in OpenAlex.

  1. Skeletal muscle alterations in Marfan syndrome: a systematic review.Journal of muscle research and cell motility · 2025
    Pooled it
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  7. The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026
    Review
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388 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 2 institutions in 1 country.

Kevin K KimDepartment of Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan 48109.
Dean SheppardDepartment of Medicine, Cardiovascular Research Institute, and Lung Biology Center, University of California, San Francisco, San Francisco, California 94143.
Harold A ChapmanDepartment of Medicine, Cardiovascular Research Institute, and Lung Biology Center, University of California, San Francisco, San Francisco, California 94143.
University of California, San Francisco · USUniversity of Michigan–Ann Arbor · US

Funding

Targeting Epithelial Cells To Treat Pulmonary FibrosisP01HL108794 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PAPA, FEROZ R · 2012 to 2016
$12.6M
REGULATION OF INTEGRIN FUNCTIONR01HL044712 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 1991 to 2014
$4.8M
Type I collagen signaling in lung injury and fibrosisR01HL108904 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIM, KEVIN KEEWOUN · 2012 to 2020
$3.5M
NHLBI NIH HHS P01 HL108794NHLBI NIH HHS R01 HL044712NHLBI NIH HHS R01 HL108904
6 · The paper itself

Abstract

Activation of TGF-β1 initiates a program of temporary collagen accumulation important to wound repair in many organs. However, the outcome of temporary extracellular matrix strengthening all too frequently morphs into progressive fibrosis, contributing to morbidity and mortality worldwide. To avoid this maladaptive outcome, TGF-β1 signaling is regulated at numerous levels and intimately connected to feedback signals that limit accumulation. Here, we examine the current understanding of the core functions of TGF-β1 in promoting collagen accumulation, parallel pathways that promote physiological repair, and pathological triggers that tip the balance toward progressive fibrosis. Implicit in better understanding of these processes is the identification of therapeutic opportunities that will need to be further advanced to limit or reverse organ fibrosis.

Indexed as

AnimalsApoptosisCell ProliferationCollagenEpithelial-Mesenchymal TransitionFeedback, PhysiologicalFibrosisHumansIntegrinsMiceModels, BiologicalSignal TransductionTransforming Growth Factor beta1Wound HealingCollagenIntegrinsTransforming Growth Factor beta1

Identifiers

PMID28432134
PMCPMC5880172
OpenAlexW2606062902

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.