Evidence map›Paper›PMID 14694243›Full record

ArticleThorax2004

Reduction of bleomycin induced lung fibrosis by candesartan cilexetil, an angiotensin II type 1 receptor antagonist.

M Otsuka, H Takahashi, M Shiratori, H Chiba, S Abe

Open access · bronzeAbstract read
In one paragraph

Article in Thorax, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Article
  8. [Surgical treatment of arthrofibrosis of the knee joint].Unfallchirurgie (Heidelberg, Germany) · 2022
    Review
  9. Article
  10. Review
  11. Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020
    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

5 authors at 1 institution in 1 country.

M OtsukaThird Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan.
H Takahashi
M Shiratori
H Chiba
S Abe
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignalling of angiotensin II via angiotensin II type 1 receptor (AT1) promotes cardiac and renal fibrosis, but its role in lung fibrosis is little understood. Using a rat bleomycin (BLM) induced model of pulmonary fibrosis, we examined the expression of AT1 in the lung and the effect of an AT1 antagonist on pulmonary fibrosis.

methodsAdult male Sprague-Dawley rats were given 0.3 mg/kg BLM intratracheally. Two days earlier they had received 10 mg/kg/day of the AT1 antagonist candesartan cilexetil mixed in the drinking water. AT1 expression in the lungs was examined by immunohistochemistry and immunoblot methods. The effect of the AT1 antagonist on pulmonary fibrosis was studied by analysis of bronchoalveolar lavage (BAL) fluid, histopathology, and hydroxyproline assay.

resultsImmunohistochemical studies showed overexpression of AT1 in inflammatory immune cells, alveolar type II cells, and fibroblasts. A quantitative assay for AT1 showed that AT1 expression was significantly upregulated in cells from BAL fluid after day 3 and in the lung homogenates after day 21. Candesartan cilexetil significantly inhibited the increase in total protein and albumin, as well as the increase in total cells and neutrophils in BAL fluid. On day 21 candesartan cilexetil also ameliorated morphological changes and an increased amount of hydroxyproline in lung homogenates. In addition, BLM increased the expression of transforming growth factor (TGF)-beta1 in BAL fluid on day 7; this increase was significantly reduced by candesartan cilexetil.

conclusionAT1 expression is upregulated in fibrotic lungs. Angiotensin II promotes lung fibrosis via AT1 and, presumably, in part via TGF-beta1.

Indexed as

Angiotensin II Type 1 Receptor BlockersTetrazolesAlbuminsAnimalsAntibiotics, AntineoplasticBenzimidazolesBiphenyl CompoundsBleomycinBlotting, WesternBronchoalveolar Lavage FluidHydroxyprolineImmunohistochemistryMaleProteinsPulmonary FibrosisRatsAlbuminsAngiotensin II Type 1 Receptor BlockersAntibiotics, AntineoplasticBenzimidazolesBiphenyl CompoundsBleomycincandesartan cilexetilHydroxyprolineProteinsReceptor, Angiotensin, Type 1TetrazolesTgfb1 protein, ratTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID14694243
PMCPMC1758867
OpenAlexW2171075888

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.