Evidence map›Paper›PMID 25559763›Full record

ArticleBritish journal of pharmacology2015

Angiotensin-(1-7) attenuates airway remodelling and hyperresponsiveness in a model of chronic allergic lung inflammation.

G S Magalhães, M G Rodrigues-Machado, D Motta-Santos, A R Silva, M V Caliari, L O Prata, S C Abreu, P R M Rocco, L S Barcelos, R A S Santos and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

49 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  3. Angiotensin-(1-7) treatment improves pneumonia and prevents sepsis caused by pneumococcal infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  11. Association Between ACE2 and Lung Diseases.Infection and drug resistance · 2024
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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

11 authors at 3 institutions in 3 countries.

G S MagalhãesDepartment of Physiology and Biophysics, National Institute of Science and Technology in Nanobiopharmaceutics (INCT-NANOBIOFAR), Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
M G Rodrigues-Machado
D Motta-Santos
A R Silva
M V Caliari
L O Prata
S C Abreu
P R M Rocco
L S Barcelos
R A S Santos
M J Campagnole-Santos
National Institute of Science and Technology · IDUniversidade Federal de Minas Gerais · BRCzech Academy of Sciences, Institute of Biophysics · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeA long-term imbalance between pro- and anti-inflammatory mediators leads to airway remodelling, which is strongly correlated to most of the symptoms, severity and progression of chronic lung inflammation. The Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis of the renin-angiotensin system is associated with attenuation of acute and chronic inflammatory processes. In this study, we investigated the effects of Ang-(1-7) treatment in a model of chronic allergic lung inflammation. EXPERIMENTAL APPROACH: Mice were sensitized to ovalbumin (OVA; 4 injections over 42 days, 14 days apart) and were challenged three times per week (days 21-46). These mice received Ang-(1-7) (1 μg·h(-1) , s.c.) by osmotic mini-pumps, for the last 28 days. Histology and morphometric analysis were performed in left lung and right ventricle. Airway responsiveness to methacholine, analysis of Ang-(1-7) levels (RIA), collagen I and III (qRT-PCR), ERK1/2 and JNK (Western blotting), IgE (elisa), cytokines and chemokines (elisa multiplex), and immunohistochemistry for Mas receptors were performed. KEY

resultsInfusion of Ang-(1-7) in OVA-sensitized and challenged mice decreased inflammatory cell infiltration and collagen deposition in the airways and lung parenchyma, and prevented bronchial hyperresponsiveness. These effects were accompanied by decreased IgE and ERK1/2 phosphorylation, and decreased pro-inflammatory cytokines. Mas receptors were detected in the epithelium and bronchial smooth muscle, suggesting a site in the lung for the beneficial actions of Ang-(1-7). CONCLUSIONS AND IMPLICATIONS: Ang-(1-7) exerted beneficial attenuation of three major features of chronic asthma: lung inflammation, airway remodelling and hyperresponsiveness. Our results support an important protective role of Ang-(1-7) in lung inflammation.

Indexed as

Airway RemodelingAngiotensin IAnimalsAnti-Inflammatory AgentsBronchial HyperreactivityBronchoconstrictionCollagenCytokinesDisease Models, AnimalHypertrophy, Right VentricularImmunoglobulin EInflammation MediatorsLungMaleMice, Inbred BALB CMitogen-Activated Protein Kinase 1Angiotensin Iangiotensin I (1-7)Anti-Inflammatory AgentsCollagenCytokinesImmunoglobulin EInflammation MediatorsMapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3OvalbuminPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID25559763
PMCPMC4403097
OpenAlexW2115006322

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.