Evidence map›Paper›PMID 17332483›Full record

ArticleAmerican journal of respiratory and critical care medicine2007

Impairment of alveolar macrophage transcription in idiopathic pulmonary fibrosis.

Ping Ren, Ivan O Rosas, Sandra D Macdonald, Hai-Ping Wu, Eric M Billings, Bernadette R Gochuico

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  3. CBClinical and translational medicine · 2021
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  12. Dysregulation of galectin-3. Implications for Hermansky-Pudlak syndrome pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Alveolar macrophage dysregulation in Hermansky-Pudlak syndrome type 1.American journal of respiratory and critical care medicine · 2009
    Article
  19. Abnormal lymphangiogenesis in idiopathic pulmonary fibrosis with insights into cellular and molecular mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

6 authors at 3 institutions in 1 country.

Ping RenPulmonary--Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Ivan O Rosas
Sandra D Macdonald
Hai-Ping Wu
Eric M Billings
Bernadette R Gochuico
Pulmonary and Critical Care Associates · USNational Institutes of Health · USNational Heart Lung and Blood Institute · US

Funding

Interstitial Lung DiseaseZ01HL002543 · NHLBI · HEART, LUNG, AND BLOOD INSTITUTE · PI GOCHUICO, BERNADETTE R · 1999 to 2006
–
Intramural NIH HHS
6 · The paper itself

Abstract

rationaleAlveolar macrophages are inflammatory cells that may contribute to the pathogenesis of idiopathic pulmonary fibrosis (IPF), which is characterized by excessive alveolar aggregation of cells and extracellular matrix proteins.

objectivesTo identify potential molecular mechanisms of IPF.

methodsTo examine large-scale gene expression, messenger RNA isolated from alveolar macrophages and peripheral blood mononuclear cells from subjects with IPF and normal volunteers was hybridized to cDNA filters. MEASUREMENTS AND MAIN

resultsWe showed that in IPF there is global down-regulation of gene expression in alveolar macrophages but not in blood monocytes. Nuclear run-on and pulse-chase studies showed that alveolar macrophages had significantly reduced transcription (p < 0.01). No significant difference in RNA degradation was found between subjects with IPF and normal volunteers. Western blot analyses revealed that concentrations of transcription factor II-H, a general transcription factor, were significantly lower in alveolar macrophages from subjects with IPF than in those from normal volunteers (p = 0.012).

conclusionsImpaired transcription in IPF is associated with decreased concentrations of transcription factor II-H in alveolar macrophages and may alter the intraalveolar milieu in IPF.

Indexed as

RNA StabilityTranscription, GeneticBiomarkersBlotting, NorthernBlotting, WesternDisease ProgressionDown-RegulationHumansMacrophages, AlveolarMonocytesPulmonary FibrosisRNA, MessengerTranscription Factor TFIIHBiomarkersRNA, MessengerTranscription Factor TFIIH

Identifiers

PMID17332483
PMCPMC1899274
OpenAlexW1970876784

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.