Evidence map›Paper›PMID 23457188›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013

Gene expression profiles reveal molecular mechanisms involved in the progression and resolution of bleomycin-induced lung fibrosis.

Sandra Cabrera, Moises Selman, Alfredo Lonzano-Bolaños, Kazuhisa Konishi, Thomas J Richards, Naftali Kaminski, Annie Pardo

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Effect ofJournal of experimental pharmacology · 2024
    Article
  5. Article
  6. Article
  7. TIMP-1 and its potential diagnostic and prognostic value in pulmonary diseases.Chinese medical journal pulmonary and critical care medicine · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Loss of MT1-MMP in Alveolar Epithelial Cells Exacerbates Pulmonary Fibrosis.International journal of molecular sciences · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Demystifying pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  18. Article
  19. Article
  20. Review
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 3 institutions in 2 countries.

Sandra CabreraFacultad de Ciencias, Universidad Nacional Autónoma de México, México DF, México.
Moises Selman
Alfredo Lonzano-Bolaños
Kazuhisa Konishi
Thomas J Richards
Naftali Kaminski
Annie Pardo
University of Pittsburgh · USInstituto Nacional de Enfermedades Respiratorias · MXUniversidad Nacional Autónoma de México · MX

Funding

Gene networks beyond organ boundaries; heart, lung and pulmonary vascular diseaseU01HL108642 · NHLBI · YALE UNIVERSITY · PI AHMAD, FERHAAN, BENOS, PANAGIOTIS V · 2011 to 2014
$2.2M
NHLBI NIH HHS U01 HL108642
6 · The paper itself

Abstract

Lung fibrosis is the final result of a large number of disorders and is usually considered an irreversible process. However, some evidence suggests that fibrosis could eventually be reversible. In this study we aimed to document the time-related reversibility of bleomycin-induced lung fibrosis and to examine the gene expression profile associated with its initial progression and subsequent resolution. C57BL/6 mice were instilled with a single dose of bleomycin and euthanized at 1, 4, 8, 12, and 16 wk. Control animals received an equal volume of saline. Lung fibrosis was examined by morphology and hydroxyproline content and the transcriptional signature by gene microarray analysis. Our results showed that bleomycin-injured mice developed prominent inflammation at 1 wk, followed by fibrosis that peaked at 2 mo. Then fibrosis resolved until lungs displayed almost normal architecture at 4 mo. Genomewide transcriptional profiling revealed 533 significantly changed genes. Self-organizing maps analysis of these genes identified four clusters based on the temporal pattern of gene expression. Clusters 1 and 2 contained genes upregulated during the inflammatory and fibrotic response and were enriched for extracellular matrix-related genes including several collagens, matrix metalloproteinases, and TIMP-1. Cluster 3 identified upregulated genes during the fibrotic response, and cluster 4 contained genes decreased during inflammation and fibrosis that increased during resolution. Most enriched pathways included genes involved in cell cycle and in regulation of transcription. Our findings corroborate the reversibility of bleomycin-induced lung fibrosis and reveal transcriptional signatures that characterize the progression and resolution.

Indexed as

BleomycinTranscriptomeAnimalsExtracellular Matrix ProteinsInflammationMiceMice, Inbred C57BLNF-kappa BPulmonary FibrosisUp-RegulationBleomycinExtracellular Matrix ProteinsNF-kappa Bfibrosis resolutionMMPSNFκB2pulmonary fibrosis

Identifiers

PMID23457188
PMCPMC4116413
OpenAlexW2160416855

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.