Evidence map›Paper›PMID 16601095›Full record

ArticleThorax2006

Losartan attenuates bleomycin induced lung fibrosis by increasing prostaglandin E2 synthesis.

M Molina-Molina, A Serrano-Mollar, O Bulbena, L Fernandez-Zabalegui, D Closa, A Marin-Arguedas, A Torrego, J Mullol, C Picado, A Xaubet

Open access · bronzeAbstract read
In one paragraph

Article in Thorax, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.8field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  6. Article
  7. Sartan-induced interstitial lung disease.Respiratory medicine case reports · 2023
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  8. Metabolic reprogramming of pulmonary fibrosis.Frontiers in pharmacology · 2022
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  15. Article
  16. Animal models of systemic sclerosis: their utility and limitations.Open access rheumatology : research and reviews · 2014
    Review
  17. Article
  18. Article
  19. Inhalation treatment of pulmonary fibrosis by liposomal prostaglandin E2.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2013
    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

10 authors at 1 institution in 1 country.

M Molina-MolinaServei de Pneumologia, Institut Clínic del Tórax, Hospital Clínic, c/Villarroel 170, Barcelona 08036, Spain. mariamolinamolina@hotmail.com
A Serrano-Mollar
O Bulbena
L Fernandez-Zabalegui
D Closa
A Marin-Arguedas
A Torrego
J Mullol
C Picado
A Xaubet
Hospital Clínic de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe angiotensin system has a role in the pathogenesis of pulmonary fibrosis. This study examines the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in bleomycin induced lung fibrosis and its possible implication in the regulation of prostaglandin E(2) (PGE(2)) synthesis and cyclooxygenase-2 (COX-2) expression.

methodsRats were given a single intratracheal instillation of bleomycin (2.5 U/kg). Losartan (50 mg/kg/day) was administrated orally starting one day before induction of lung fibrosis and continuing to the conclusion of each experiment.

resultsLosartan reduced the inflammation induced by bleomycin, as indicated by lower myeloperoxidase activity and protein content in the bronchoalveolar lavage fluid. Collagen deposition induced by bleomycin was inhibited by losartan, as shown by a reduction in the hydroxyproline content and the amelioration of morphological changes. PGE(2) levels were lower in fibrotic lungs than in normal lungs. Losartan significantly increased PGE(2) levels at both 3 and 15 days. A reduction in COX-2 expression by bleomycin was seen at 3 days which was relieved by losartan.

conclusionsThe antifibrotic effect of losartan appears to be mediated by its ability to stimulate the production of PGE(2). Losartan, which is already widely used clinically, could be assessed as a new treatment in lung fibrosis.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsAntimetabolites, AntineoplasticBleomycinCyclooxygenase 2DinoprostoneLosartanMalePulmonary FibrosisRandom AllocationRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionAngiotensin II Type 1 Receptor BlockersAntimetabolites, AntineoplasticBleomycinCyclooxygenase 2DinoprostoneLosartan

Identifiers

PMID16601095
PMCPMC2104675
OpenAlexW2109894557

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.