Evidence map›Paper›PMID 32067272›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

IPF pathogenesis is dependent upon TGFβ induction of IGF-1.

Danielle M Hernandez, Jeong-Han Kang, Malay Choudhury, Mahefatiana Andrianifahanana, Xueqian Yin, Andrew H Limper, Edward B Leof

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 63 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Inter-Organ Communication in Pulmonary Fibrosis: Systemic Modifiers of a Lung-Centered Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Article
  5. Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. The IGF System and Aging.Endocrine reviews · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. GTSE1-driven ZEB1 stabilization promotes pulmonary fibrosis through the epithelial-to-mesenchymal transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  15. Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Danielle M HernandezMayo Clinic Graduate School of Biomedical Sciences, Biochemistry & Molecular Biology Department, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.
Jeong-Han KangThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Malay ChoudhuryThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Mahefatiana AndrianifahananaThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Xueqian YinThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Andrew H LimperThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Edward B LeofThoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
TGF BETA RECEPTORS AND CELL PROLIFERATIONR01GM054200 · NIGMS · MAYO CLINIC ROCHESTER · PI LEOF, EDWARD B · 1996 to 2018
$6.1M
TGF Beta Receptor DynamicsR37GM055816 · NIGMS · MAYO CLINIC ROCHESTER · PI LEOF, EDWARD B · 2009 to 2018
$3.6M
NCI NIH HHS P30 CA014520NIGMS NIH HHS R01 GM054200NIGMS NIH HHS R37 GM055816
6 · The paper itself

Abstract

Pathogenic fibrotic diseases, including idiopathic pulmonary fibrosis (IPF), have some of the worst prognoses and affect millions of people worldwide. With unclear etiology and minimally effective therapies, two-thirds of IPF patients die within 2-5 years from this progressive interstitial lung disease. Transforming Growth Factor Beta (TGFβ) and insulin-like growth factor-1 (IGF-1) are known to promote fibrosis; however, myofibroblast specific upregulation of IGF-1 in the initiation and progression of TGFβ-induced fibrogenesis and IPF have remained unexplored. To address this, the current study (1) documents the upregulation of IGF-1 via TGFβ in myofibroblasts and fibrotic lung tissue, as well as its correlation with decreased pulmonary function in advanced IPF; (2) identifies IGF-1's C1 promoter as mediating the increase in IGF-1 transcription by TGFβ in pulmonary fibroblasts; (3) determines that SMAD2 and mTOR signaling are required for TGFβ-dependent Igf-1 expression in myofibroblasts; (4) demonstrates IGF-1R activation is essential to support TGFβ-driven profibrotic myofibroblast functions and excessive wound healing; and (5) establishes the effectiveness of slowing the progression of murine lung fibrosis with the IGF-1R inhibitor OSI-906. These findings expand our knowledge of IGF-1's role as a novel fibrotic-switch, bringing us one step closer to understanding the complex biological mechanisms responsible for fibrotic diseases and developing effective therapies.

Indexed as

AnimalsAntibiotics, AntineoplasticBleomycinCell DifferentiationCells, CulturedFibroblastsIdiopathic Pulmonary FibrosisInsulin-Like Growth Factor IMaleMiceMice, Inbred C57BLTransforming Growth Factor betaAntibiotics, AntineoplasticBleomycinInsulin-Like Growth Factor ITransforming Growth Factor betafibroblastpromotersignalingtranscription

Identifiers

PMID32067272
PMCPMC7136152
OpenAlexW3008667790

What OpenQuestion holds

Textmetadata
LicenceTDM
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.