Evidence map›Paper›PMID 24098808›Full record

ArticlePloS one2013

Mechanisms involved in the beneficial effects of spironolactone after myocardial infarction.

Marcos F Minicucci, Priscila P dos Santos, Bruna P M Rafacho, Andrea F Gonçalves, Renata A C Silva, Fernanda Chiuso-Minicucci, Paula S Azevedo, Bertha F Polegato, Katashi Okoshi, Elenize J Pereira and 2 more

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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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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

12 authors at 1 institution in 1 country.

Marcos F MinicucciInternal Medicine Department, Botucatu Medical School, University Estadual Paulista, Botucatu, São Paulo, Brazil.
Priscila P dos Santos
Bruna P M Rafacho
Andrea F Gonçalves
Renata A C Silva
Fernanda Chiuso-Minicucci
Paula S Azevedo
Bertha F Polegato
Katashi Okoshi
Elenize J Pereira
Sergio A R Paiva
Leonardo A M Zornoff
Universidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOur objective was to analyze the effect of spironolactone on cardiac remodeling after experimental myocardial infarction (MI), assessed by matricellular proteins levels, cardiac collagen amount and distribution, myocardial tissue metalloproteinase inhibitor-1 (TIMP-1) concentration, myocyte hypertrophy, left ventricular architecture, and in vitro and in vivo cardiac function.

methodsWistar rats were assigned to 4 groups: control group, in which animals were submitted to simulated surgery (SHAM group; n=9); group that received spironolactone and in which animals were submitted to simulated surgery (SHAM-S group, n=9); myocardial infarction group, in which animals were submitted to coronary artery ligation (MI group, n=15); and myocardial infarction group with spironolactone supplementation (MI-S group, n=15). The rats were observed for 3 months.

resultsThe MI group had higher values of left cardiac chambers and mass index and lower relative wall thicknesses compared with the SHAM group. In addition, diastolic and systolic functions were worse in the MI groups. However, spironolactone did not influence any of these variables. The MI-S group had a lower myocardial hydroxyproline concentration and myocyte cross-sectional area compared with the MI group. Myocardial periostin and collagen type III were lower in the MI-S group compared with the MI-group. In addition, TIMP-1 concentration in myocardium was higher in the MI-S group compared with the MI group.

conclusionsThe predominant consequence of spironolactone supplementation after MI is related to reductions in collagens, with discrete attenuation of other remodeling variables. Importantly, this effect may be modulated by periostin and TIMP-1 levels.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternBody Weights and MeasuresCollagenEchocardiographyHydroxyprolineMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mineralocorticoid Receptor AntagonistsMuscle CellsMyocardial InfarctionRatsRats, WistarSpironolactoneCollagenHydroxyprolineMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mineralocorticoid Receptor AntagonistsSpironolactoneTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID24098808
PMCPMC3786966
OpenAlexW2003212233

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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.