Evidence map›Paper›PMID 23889691›Full record

ArticleBritish journal of pharmacology2013

AVE 0991, a non-peptide mimic of angiotensin-(1-7) effects, attenuates pulmonary remodelling in a model of chronic asthma.

M G Rodrigues-Machado, G S Magalhães, J A Cardoso, L M Kangussu, A Murari, M V Caliari, M L Oliveira, D C Cara, M L M Noviello, F D Marques and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 79 citations in OpenAlex.

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  8. A single dose of angiotensin-(1-7) resolves eosinophilic inflammation and protects the lungs from a secondary inflammatory challenge.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  9. Review
  10. Evaluation of cardiac function in asthmatic children by Tissue Doppler Echocardiography.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023
    Article
  11. Article
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  16. Article
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  19. Targeting the renin-angiotensin signaling pathway in COVID-19: Unanswered questions, opportunities, and challenges.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Review
  20. Review
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

14 authors at 2 institutions in 2 countries.

M G Rodrigues-MachadoNational Institute of Science and Technology in Nanobiopharmaceutics (INCT-NANOBIOFAR), Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Brazil.
G S Magalhães
J A Cardoso
L M Kangussu
A Murari
M V Caliari
M L Oliveira
D C Cara
M L M Noviello
F D Marques
J M Pereira
R Q Lautner
R A S Santos
M J Campagnole-Santos
Universidade Federal de Minas Gerais · BRNational Institute of Science and Technology · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAVE 0991 (AVE) is a non-peptide compound, mimic of the angiotensin (Ang)-(1-7) actions in many tissues and pathophysiological states. Here, we have investigated the effect of AVE on pulmonary remodelling in a murine model of ovalbumin (OVA)-induced chronic allergic lung inflammation. EXPERIMENTAL APPROACH: We used BALB/c mice (6-8 weeks old) and induced chronic allergic lung inflammation by OVA sensitization (20 μg·mouse(-1) , i.p., four times, 14 days apart) and OVA challenge (1%, nebulised during 30 min, three times per·week, for 4 weeks). Control and AVE groups were given saline i.p and challenged with saline. AVE treatment (1 mg·kg(-1) ·per day, s.c.) or saline (100 μL·kg(-1) ·per day, s.c.) was given during the challenge period. Mice were anaesthetized 72 h after the last challenge and blood and lungs collected. In some animals, primary bronchi were isolated to test contractile responses. Cytokines were evaluated in bronchoalveolar lavage (BAL) and lung homogenates. KEY

resultsTreatment with AVE of OVA sensitised and challenged mice attenuated the altered contractile response to carbachol in bronchial rings and reversed the increased airway wall and pulmonary vasculature thickness and right ventricular hypertrophy. Furthermore, AVE reduced IL-5 and increased IL-10 levels in the BAL, accompanied by decreased Ang II levels in lungs. CONCLUSIONS AND IMPLICATIONS: AVE treatment prevented pulmonary remodelling, inflammation and right ventricular hypertrophy in OVA mice, suggesting that Ang-(1-7) receptor agonists are a new possibility for the treatment of pulmonary remodelling induced by chronic asthma.

Indexed as

Airway RemodelingAngiotensin IAngiotensin IIAnimalsAnti-Asthmatic AgentsAsthmaBronchoalveolar Lavage FluidBronchoconstrictionChronic DiseaseCytokinesDisease Models, AnimalHypertrophy, Right VentricularImidazolesLungMaleMiceAngiotensin Iangiotensin I (1-7)Angiotensin IIAnti-Asthmatic AgentsAVE 0991CytokinesImidazolesOvalbuminPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledairway remodellingallergic lung inflammationangiotensin-(1-7)asthmaAVE 0991cytokinesMas receptor

Identifiers

PMID23889691
PMCPMC3799597
OpenAlexW1538839647

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.