Evidence map›Paper›PMID 15491504›Full record

ReviewJournal of cellular and molecular medicine

The central role of Fas-ligand cell signaling in inflammatory lung diseases.

G A Dosreis, Valeria M Borges, W A Zin

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 61 citations in OpenAlex.

  1. The role of inflammation in silicosis.Frontiers in pharmacology · 2024
    Review
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  7. The anesthetic agent sevoflurane attenuates pulmonary acute lung injury by modulating apoptotic pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
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  16. An overview of caspase: Apoptotic protein for silicosis.Indian journal of occupational and environmental medicine · 2010
    Article
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  19. Calcium and ER stress mediate hepatic apoptosis after burn injury.Journal of cellular and molecular medicine · 2009
    Article
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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 2 institutions in 2 countries.

G A DosreisInstituto de Biofísica Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21949-900, Brazil. gdosreis@biof.ufrj.br
Valeria M Borges
W A Zin
Universidade Federal do Rio de Janeiro · BRFundação Oswaldo Cruz · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following inflammation and injury in the lung, loss of epithelial cell precursors could determine the balance between tissue regeneration and fibrosis. This review discusses evidence that proapoptotic Fas-Fas ligand (FasL) signaling plays a central role in pulmonary inflammation, injury and fibrosis. FasL signaling induces inflammatory apoptosis in epithelial cells and alveolar macrophages, with concomitant IL-1 beta and chemokine release, leading to neutrophil infiltration. FasL signaling plays a critical role in models of acute lung injury, idiopathic pulmonary fibrosis and silicosis; blockade of Fas-FasL interactions either prevents or attenuates pulmonary inflammation and fibrosis. Serologic and immunohistochemical studies in patients support a major pathogenic role of Fas and FasL molecules in inflammatory lung diseases. Identification of the pathogenic role of FasL could facilitate the discovery of more effective treatments for currently untreatable inflammatory lung diseases.

Indexed as

Acute DiseaseApoptosisEpithelial CellsFas Ligand Proteinfas ReceptorGene Expression RegulationHumansInterleukin-1Macrophages, AlveolarMembrane GlycoproteinsNeutrophilsPneumoniaPulmonary AlveoliPulmonary FibrosisSignal TransductionSilicosisFASLG protein, humanFas Ligand Proteinfas ReceptorInterleukin-1Membrane Glycoproteins

Identifiers

PMID15491504
PMCPMC6740074
OpenAlexW2103264487

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.