Evidence map›Paper›PMID 26715125›Full record

ArticleTherapeutic advances in cardiovascular disease2016

Cardiac ACE2/angiotensin 1-7/Mas receptor axis is activated in thyroid hormone-induced cardiac hypertrophy.

Gabriela P Diniz, Nathalia Senger, Marcela S Carneiro-Ramos, Robson A S Santos, Maria Luiza M Barreto-Chaves

Open access · bronzeAbstract read
In one paragraph

Article in Therapeutic advances in cardiovascular disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. COVID-19 and Thyroid Diseases: A Bidirectional Impact.Journal of the Endocrine Society · 2021
    Review
  7. Review
  8. Review
  9. Endocrine Conditions and COVID-19.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020
    Review
  10. Review
  11. 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

5 authors at 3 institutions in 2 countries.

Gabriela P DinizDepartment of Anatomy, Laboratory of Cell Biology and Functional Anatomy, University of São Paulo, Sao Paulo, Brazil.
Nathalia SengerDepartment of Anatomy, Laboratory of Cell Biology and Functional Anatomy, University of São Paulo, Sao Paulo, Brazil.
Marcela S Carneiro-RamosHuman and Natural Sciences Center, Federal University of ABC, São Paulo, Brazil.
Robson A S SantosDepartment of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, BrazilCardiology Institute of Rio Grande do Sul, University Foundation of Cardiology.
Maria Luiza M Barreto-ChavesLaboratory of Cellular Biology and Functional Anatomy, Department of Anatomy, Biomedical Sciences Institute, University of São Paulo, Av. Prof. Lineu Prestes 2415, Cidade Universitária, São Paulo, SP 05508-900, Brazil mchaves@usp.br.
Universidade de São Paulo · BRUniversidade Federal do ABC · BRUniversity Foundation · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThyroid hormone (TH) promotes marked effects on the cardiovascular system, including the development of cardiac hypertrophy. Some studies have demonstrated that the renin-angiotensin system (RAS) is a key mediator of the cardiac growth in response to elevated TH levels. Although some of the main RAS components are changed in cardiac tissue on hyperthyroid state, the potential modulation of the counter regulatory components of the RAS, such as angiotensin-converting enzyme type 2 (ACE2), angiotensin 1-7 (Ang 1-7) levels and Mas receptor induced by hyperthyroidism is unknown. The aim of this study was to investigate the effect of hyperthyroidism on cardiac Ang 1-7, ACE2 and Mas receptor levels.

methodsHyperthyroidism was induced in Wistar rats by daily intraperitoneal injections of T4 for 14 days.

resultsAlthough plasma Ang 1-7 levels were unchanged by hyperthyroidism, cardiac Ang 1-7 levels were increased in TH-induced cardiac hypertrophy. ACE2 enzymatic activity was significantly increased in hearts from hyperthyroid animals, which may be contributing to the higher Ang 1-7 levels observed in the T4 group. Furthermore, elevated cardiac levels of Ang 1-7 levels were accompanied by increased Mas receptor protein levels.

conclusionThe counter-regulatory components of the RAS are activated in hyperthyroidism and may be contributing to modulate the cardiac hypertrophy in response to TH.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAnimalsCardiomegalyHyperthyroidismMaleMyocardiumPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsRatsRats, WistarReceptors, G-Protein-CoupledRenin-Angiotensin SystemACE2 protein, humanAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Peptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledangiotensin 1–7angiotensin-converting enzyme type 2Mas receptorthyroid hormone

Identifiers

PMID26715125
PMCPMC5942623
OpenAlexW2341413642

What OpenQuestion holds

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Registered trials

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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.