Evidence map›Paper›PMID 18162602›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008

PPAR-gamma agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis.

Jami E Milam, Venkateshwar G Keshamouni, Sem H Phan, Biao Hu, Srinivasa R Gangireddy, Cory M Hogaboam, Theodore J Standiford, Victor J Thannickal, Raju C Reddy

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
–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.

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

127 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  7. 12/15-lipoxygenase orchestrates murine wound healing via PPARγ-activating oxylipins acting holistically to dampen inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

67 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

9 authors.

Jami E MilamUniv. of Michigan, Division of Pulmonary and Critical Care Medicine, 109 Zina Pitcher Pl., 4062 BSRB, Ann Arbor, MI 48109-2200, USA.
Venkateshwar G Keshamouni
Sem H Phan
Biao Hu
Srinivasa R Gangireddy
Cory M Hogaboam
Theodore J Standiford
Victor J Thannickal
Raju C Reddy

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
SCCOR in Translational Research in Acute Lung InjuryP50HL074024 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KUNKEL, STEVEN LYNN · 2003 to 2007
$13.5M
MYOFIBROBLASTS IN PULMONARY FIBROSISR01HL052285 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1994 to 2017
$5.4M
SCOR ON ACUTE LUNG INJURYP50HL060289 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STANDIFORD, THEODORE J. · 1999 to 2003
$4.2M
PPARGamma in Sepsis-Induced ImmunosuppressionK08HL070068 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI REDDY, RAJU C · 2002 to 2006
$663k
NHLBI NIH HHS HL-52285NHLBI NIH HHS HL-70068NHLBI NIH HHS K08 HL070068NHLBI NIH HHS P50 HL074024NHLBI NIH HHS P50 HL-60289NHLBI NIH HHS P50 HL-74024NHLBI NIH HHS R01 HL052285NHLBI NIH HHS T32 HL007749
6 · The paper itself

Abstract

Pulmonary fibrosis is characterized by alterations in fibroblast phenotypes resulting in excessive extracellular matrix accumulation and anatomic remodeling. Current therapies for this condition are largely ineffective. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the nuclear hormone receptor superfamily, the activation of which produces a number of biological effects, including alterations in metabolic and inflammatory responses. The role of PPAR-gamma as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-gamma in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-gamma agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-gamma agonists, including a constitutively active PPAR-gamma construct (VP16-PPAR-gamma), inhibit the ability of transforming growth factor-beta1 to induce myofibroblast differentiation and collagen secretion. PPAR-gamma agonists also inhibit fibrosis in a murine model, even when administration is delayed until after the initial inflammation has largely resolved. These observations indicate that PPAR-gamma is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-gamma ligands as novel therapeutic agents for fibrotic lung diseases.

Indexed as

AnimalsAntibiotics, AntineoplasticBleomycinCell DifferentiationCell DivisionCells, CulturedChromansCyclin DCyclinsDisease Models, AnimalFibroblastsFibrosisGene ExpressionHumansHypoglycemic AgentsLigandsAntibiotics, AntineoplasticBleomycinChromansciglitazoneCyclin DCyclinsHypoglycemic AgentsLigandsPPAR gammaThiazolidinedionesTransforming Growth Factor beta1Troglitazone

Identifiers

PMID18162602
PMCPMC5926773

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.