Evidence map›Paper›PMID 23885794›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

Endothelial cells recruit macrophages and contribute to a fibrotic milieu in bleomycin lung injury.

Heather G Leach, Izabela Chrobak, Rong Han, Maria Trojanowska

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

55 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
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  8. Article
  9. The role of vascularity and the fibrovascular interface in interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  10. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023
    Review
  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

4 authors at 1 institution in 1 country.

Heather G Leach1 Department of Pathology, and.
Izabela Chrobak
Rong Han
Maria Trojanowska
Boston University · US

Funding

Translational studies for identifying and targeting novel pathways in systemic sclerosis pathogenesisP50AR060780 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2011 to 2021
$14.9M
The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
RHEUMATOLOGY TRAINING GRANTT32AR007598 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FELSON, DAVID TOBIN · 1997 to 2018
$2.3M
NIAMS NIH HHS AR042334NIAMS NIH HHS P50 AR060780NIAMS NIH HHS R01 AR042334NIAMS NIH HHS T32 AR007598
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a systemic autoimmune disease that causes inflammation, vasculopathy, and fibrosis of the skin and internal organs. One of the most severe complications of SSc involves the development of pulmonary fibrosis. Endothelial cell injury precedes the development of fibrosis, and is believed to be an initiating event. Therefore, we aimed to characterize the role of endothelial cells in the progression of pulmonary fibrosis, using a well-established bleomycin (BLM) model of pulmonary fibrosis. Endothelial cells were isolated by cell sorting, and the analysis of gene expression was performed with quantitative RT-PCR. Endothelial injury was induced between the first and second week, as shown by the elevated expression of the vascular injury markers matrix metallopeptidase-12 and von Willebrand factor. After injury, endothelial activation was indicated by the up-regulation of selectins, CCL chemokines, and inflammatory mediators, including complement anaphylatoxin receptors (C3aR and C5aR), oncostatin M, and leukemia inhibitory factor. The endothelial cell overexpression of fibrotic mediators, including connective tissue growth factor, plasminogen activator inhibitor-1, osteopontin, fibronectin, and fibroblast specific protein-1, was observed in the second and fourth weeks. This study suggests that endothelial cells actively contribute to the disease process via multiple mechanisms, including the recruitment of inflammatory cells and the establishment of a profibrotic environment during the development of BLM-induced pulmonary fibrosis.

Indexed as

AnimalsBleomycinChemokinesDisease Models, AnimalEndothelial CellsInflammation MediatorsLung InjuryMacrophagesMaleMiceMice, Inbred C57BLPulmonary FibrosisScleroderma, SystemicSelectinsUp-RegulationBleomycinChemokinesInflammation MediatorsSelectins

Identifiers

PMID23885794
PMCPMC3931119
OpenAlexW2029081826

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.