Evidence map›Paper›PMID 23762470›Full record

ArticlePloS one2013

Beneficial effects of the activation of the angiotensin-(1-7) MAS receptor in a murine model of adriamycin-induced nephropathy.

Kátia Daniela Silveira, Lívia Corrêa Barroso, Angélica Thomáz Vieira, Daniel Cisalpino, Cristiano Xavier Lima, Michael Bader, Rosa Maria Esteves Arantes, Robson Augusto Souza Dos Santos, Ana Cristina Simões-E-Silva, Mauro Martins Teixeira

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Kátia Daniela SilveiraImunofarmacologia, Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Lívia Corrêa Barroso
Angélica Thomáz Vieira
Daniel Cisalpino
Cristiano Xavier Lima
Michael Bader
Rosa Maria Esteves Arantes
Robson Augusto Souza Dos Santos
Ana Cristina Simões-E-Silva
Mauro Martins Teixeira
Universidade Federal de Minas Gerais · BRMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin-(1-7) [Ang-(1-7)] is a biologically active heptapeptide that may counterbalance the physiological actions of angiotensin II (Ang II) within the renin-angiotensin system (RAS). Here, we evaluated whether activation of the Mas receptor with the oral agonist, AVE 0991, would have renoprotective effects in a model of adriamycin (ADR)-induced nephropathy. We also evaluated whether the Mas receptor contributed for the protective effects of treatment with AT1 receptor blockers. ADR (10 mg/kg) induced significant renal injury and dysfunction that was maximal at day 14 after injection. Treatment with the Mas receptor agonist AVE 0991 improved renal function parameters, reduced urinary protein loss and attenuated histological changes. Renoprotection was associated with reduction in urinary levels of TGF-β. Similar renoprotection was observed after treatment with the AT1 receptor antagonist, Losartan. AT1 and Mas receptor mRNA levels dropped after ADR administration and treatment with losartan reestablished the expression of Mas receptor and increased the expression of ACE2. ADR-induced nephropathy was similar in wild type (Mas(+/+) ) and Mas knockout (Mas (-/-)) mice, suggesting there was no endogenous role for Mas receptor activation. However, treatment with Losartan was able to reduce renal injury only in Mas(+/+) , but not in Mas (-/-) mice. Therefore, these findings suggest that exogenous activation of the Mas receptor protects from ADR-induced nephropathy and contributes to the beneficial effects of AT1 receptor blockade. Medications which target specifically the ACE2/Ang-(1-7)/Mas axis may offer new therapeutic opportunities to treat human nephropathies.

Indexed as

Angiotensin IAngiotensin II Type 1 Receptor BlockersAnimalsDisease Models, AnimalDoxorubicinGene Expression RegulationHumansImidazolesKidney DiseasesKidney GlomerulusKidney TubulesLosartanMicePeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasAngiotensin Iangiotensin I (1-7)Angiotensin II Type 1 Receptor BlockersAVE 0991DoxorubicinImidazolesLosartanPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledRNA, Messenger

Identifiers

PMID23762470
PMCPMC3676359
OpenAlexW2033684886

What OpenQuestion holds

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LicenceCC BY
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.