Evidence map›Paper›PMID 23488800›Full record

ReviewBritish journal of pharmacology2013

ACE2, angiotensin-(1-7) and Mas receptor axis in inflammation and fibrosis.

A C Simões e Silva, K D Silveira, A J Ferreira, M M Teixeira

Abstract readReview
In one paragraph

Review 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 298 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
298citing papers in PubMed, 5 pooled it
14.2field-weighted citation impact, top 1% 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

298 citing papers in PubMed, 5 syntheses or guidelines pooled it, 535 citations in OpenAlex.

  1. Pooled it
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  15. Activation of Angiotensin-Converting Enzyme 2 Mitigates Gastrointestinal Acute Radiation Syndrome.International journal of radiation oncology, biology, physics · 2026
    Article
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  17. Article
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  19. 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
    Article
  20. Review

238 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

A C Simões e SilvaDepartamento de Pediatria, Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
K D Silveira
A J Ferreira
M M Teixeira
Faculdade de Ciências Médicas de Minas Gerais · BRUniversidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances have improved our understanding of the renin-angiotensin system (RAS). These have included the recognition that angiotensin (Ang)-(1-7) is a biologically active product of the RAS cascade. The identification of the ACE homologue ACE2, which forms Ang-(1-7) from Ang II, and the GPCR Mas as an Ang-(1-7) receptor have provided the necessary biochemical and molecular background and tools to study the biological significance of Ang-(1-7). Most available evidence supports a counter-regulatory role for Ang-(1-7) by opposing many actions of Ang II on AT₁ receptors, especially vasoconstriction and proliferation. Many studies have now shown that Ang-(1-7) by acting via Mas receptor exerts inhibitory effects on inflammation and on vascular and cellular growth mechanisms. Ang-(1-7) has also been shown to reduce key signalling pathways and molecules thought to be relevant for fibrogenesis. Here, we review recent findings related to the function of the ACE2/Ang-(1-7)/Mas axis and focus on the role of this axis in modifying processes associated with acute and chronic inflammation, including leukocyte influx, fibrogenesis and proliferation of certain cell types. More attention will be given to the involvement of the ACE2/Ang-(1-7)/Mas axis in the context of renal disease because of the known relevance of the RAS for the function of this organ and for the regulation of kidney inflammation and fibrosis. Taken together, this knowledge may help in paving the way for the development of novel treatments for chronic inflammatory and renal diseases.

Indexed as

Models, BiologicalSignal TransductionAngiotensin-Converting Enzyme 2Angiotensin IAnimalsCell ProliferationFibrosisHumansKidneyLeukocytesNephritisPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Peptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID23488800
PMCPMC3682698
OpenAlexW2138043907

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.