Evidence map›Paper›PMID 29733296›Full record

ArticleThe Journal of clinical investigation2018

FOXM1 is a critical driver of lung fibroblast activation and fibrogenesis.

Loka R Penke, Jennifer M Speth, Vijaya L Dommeti, Eric S White, Ingrid L Bergin, Marc Peters-Golden

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

21 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

6 authors at 3 institutions in 1 country.

Loka R PenkeDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine.
Jennifer M SpethDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine.
Vijaya L DommetiMichigan Center for Translational Pathology, Department of Pathology, and.
Eric S WhiteDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine.
Ingrid L BerginUnit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Marc Peters-GoldenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine.
Pulmonary and Critical Care Associates · USMichigan Center for Translational Pathology · USUniversity of Michigan · US

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Control of Fibroblast Function by Prostaglandin E2 and Plasminogen ActivationR01HL094311 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2009 to 2017
$3.4M
NHLBI NIH HHS R01 HL094311NHLBI NIH HHS T32 HL007749
6 · The paper itself

Abstract

While the transcription factor forkhead box M1 (FOXM1) is well known as a proto-oncogene, its potential role in lung fibroblast activation has never been explored. Here, we show that FOXM1 is more highly expressed in fibrotic than in normal lung fibroblasts in humans and mice. FOXM1 was required not only for cell proliferation in response to mitogens, but also for myofibroblast differentiation and apoptosis resistance elicited by TGF-β. The lipid mediator PGE2, acting via cAMP signaling, was identified as an endogenous negative regulator of FOXM1. Finally, genetic deletion of FOXM1 in fibroblasts or administration of the FOXM1 inhibitor Siomycin A in a therapeutic protocol attenuated bleomycin-induced pulmonary fibrosis. Our results identify FOXM1 as a driver of lung fibroblast activation and underscore the therapeutic potential of targeting FOXM1 for pulmonary fibrosis.

Indexed as

Second Messenger SystemsAnimalsBleomycinCell LineCell ProliferationCyclic AMPDisease Models, AnimalFemaleFibroblastsForkhead Box Protein M1HumansLungMiceMice, KnockoutPeptidesProto-Oncogene MasBleomycinCyclic AMPForkhead Box Protein M1FOXM1 protein, humanFoxm1 protein, mouseMAS1 protein, humanPeptidesProto-Oncogene Massiomycin ADrug therapyFibrosisPulmonologySignal transduction

Identifiers

PMID29733296
PMCPMC5983327
OpenAlexW2801638676

What OpenQuestion holds

Textmetadata
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.