Evidence map›Paper›PMID 19659647›Full record

ReviewRespirology (Carlton, Vic.)2009

Development, repair and fibrosis: what is common and why it matters.

Wei Shi, Jun Xu, David Warburton

Open access · bronzeAbstract readReview
In one paragraph

Review in Respirology (Carlton, Vic.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.7field-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

38 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis.Journal of the American Society of Nephrology : JASN · 2018
    Article
  10. Article
  11. Review
  12. Developmental pathways in lung regeneration.Cell and tissue research · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Secreted phosphoprotein 1 is a determinant of lung function development in mice.American journal of respiratory cell and molecular biology · 2014
    Article
  17. Article
  18. Article
  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

3 authors at 3 institutions in 2 countries.

Wei ShiDevelopmental Biology and Regenerative Medicine Program, Saban Research Institute, Childrens Hospital Los Angeles, 4650 Sunset Blvd., MS 35, Los Angeles, CA 90027, USA. wshi@chla.usc.edu
Jun Xu
David Warburton
Children's Hospital of Los Angeles · USState Key Laboratory of Respiratory Disease · CNUniversity of Southern California · US

Funding

TGF BETA SIGNALING IN LUNG MORPHOGENESIS, INJURY AND REPAIRP01HL060231 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI HEISTERKAMP, NORA C · 1998 to 2009
$14.5M
Molecular Mechanisms of Lung Branching MorphogenesisR01HL068597 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI SHI, WEI · 2002 to 2015
$4.7M
DEVELOPMENTAL TYPE II PNEUMOCYTE PROTEIN PHOSPHORYLATIONR01HL044060 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI WARBURTON, DAVID · 1991 to 2010
$3.8M
AUTOCRINE/PARACRINE GROWTH FACTORS &LUNG MORPHOGENESISR01HL044977 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WARBURTON, DAVID · 1991 to 2009
$3.3M
Lung epithelial and vascular morphogenesisR01HL075773 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI WARBURTON, DAVID · 2003 to 2006
$1.4M
NHLBI NIH HHS HL44060NHLBI NIH HHS HL44977NHLBI NIH HHS HL60231NHLBI NIH HHS HL68597NHLBI NIH HHS HL75773NHLBI NIH HHS P01 HL060231NHLBI NIH HHS R01 HL044060NHLBI NIH HHS R01 HL044977NHLBI NIH HHS R01 HL068597NHLBI NIH HHS R01 HL075773
6 · The paper itself

Abstract

The complex structure of the lung is developed sequentially, initially by epithelial tube branching and later by septation of terminal air sacs with accompanying coordinated growth of a variety of lung epithelial and mesenchymal cells. Groups of transcriptional factors, peptide growth factors and their intracellular signaling regulators, as well as extracellular matrix proteins are programmed to be expressed at appropriate levels in the right place at the right time to control normal lung formation. Studies of lung development and lung repair/fibrosis to date have discovered that many of the same factors that control normal development are also key players in lung injury repair and fibrosis. Transforming growth factor-beta (TGF-beta) family peptide signaling is a prime example. Lack of TGF-beta signaling results in abnormal lung branching morphogenesis and alveolarization during development, whereas excessive amounts of TGF-beta signaling cause severe hypoplasia in the immature lung and fibrosis in mature lung. This leads us to propose the 'Goldilocks' hypothesis of regulatory signaling in lung development and injury repair that everything must be done just right!

Indexed as

Extracellular MatrixHumansLungLung InjuryPulmonary FibrosisSignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID19659647
PMCPMC2747658
OpenAlexW1981528565

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.