Evidence map›Paper›PMID 29232407›Full record

ArticlePloS one2017

Temporal changes in cardiac oxidative stress, inflammation and remodeling induced by exercise in hypertension: Role for local angiotensin II reduction.

Sebastião D Silva, Zaira P Jara, Roseli Peres, Larissa S Lima, Cristóforo Scavone, Augusto C Montezano, Rhian M Touyz, Dulce E Casarini, Lisete C Michelini

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.6field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

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  17. Moderate Physical Exercise Activates ATRFrontiers in physiology · 2021
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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

9 authors at 3 institutions in 2 countries.

Sebastião D SilvaDepartment of Physiology & Biophysics, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil.
Zaira P JaraDepartment of Medicine, Federal University of Sao Paulo, Sao Paulo, SP, Brazil.
Roseli PeresDepartment of Medicine, Federal University of Sao Paulo, Sao Paulo, SP, Brazil.
Larissa S LimaDepartment of Pharmacology, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil.
Cristóforo ScavoneDepartment of Pharmacology, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil.
Augusto C MontezanoInstitute of Cardiovascular and Medical Sciences, BHF GCRC, University of Glasgow, Glasgow, United Kingdom.
Rhian M TouyzInstitute of Cardiovascular and Medical Sciences, BHF GCRC, University of Glasgow, Glasgow, United Kingdom.
Dulce E CasariniDepartment of Medicine, Federal University of Sao Paulo, Sao Paulo, SP, Brazil.
Lisete C MicheliniDepartment of Physiology & Biophysics, Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil.ORCID http://orcid.org/0000-0003-2978-5406
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BRUniversity of Glasgow · GB

Funding

British Heart Foundation RG/13/7/30099
6 · The paper itself

Abstract

Exercise training reduces renin-angiotensin system (RAS) activation, decreases plasma and tissue oxidative stress and inflammation in hypertension. However, the temporal nature of these phenomena in response to exercise is unknown. We sought to determine in spontaneously hypertensive rats (SHR) and age-matched WKY controls the weekly effects of training on blood pressure (BP), plasma and left ventricle (LV) Ang II and Ang-(1-7) content (HPLC), LV oxidative stress (DHE staining), gene and protein expression (qPCR and WB) of pro-inflammatory cytokines, antioxidant enzymes and their consequence on hypertension-induced cardiac remodeling. SHR and WKY were submitted to aerobic training (T) or maintained sedentary (S) for 8 weeks; measurements were made at weeks 0, 1, 2, 4 and 8. Hypertension-induced cardiac hypertrophy was accompanied by acute plasma Ang II increase with amplified responses during the late phase of LV hypertrophy. Similar pattern was observed for oxidative stress markers, TNF alpha and interleukin-1β, associated with cardiomyocytes' diameter enlargement and collagen deposition. SHR-T exhibited prompt and marked decrease in LV Ang II content (T1 vs T4 in WKY-T), normalized oxidative stress (T2), augmented antioxidant defense (T4) and reduced both collagen deposition and inflammatory profile (T8), without changing cardiomyocytes' diameter and LV hypertrophy. These changes were accompanied by decreased plasma Ang II content (T2-T4) and reduced BP (T8). SHR-T and WKY-T showed parallel increases in LV and plasma Ang-(1-7) content. Our data indicate that early training-induced downregulation of LV ACE-AngII-AT1 receptor axis is a crucial mechanism to reduce oxidative/pro-inflammatory profile and improve antioxidant defense in SHR-T, showing in addition this effect precedes plasma RAS deactivation.

Indexed as

Oxidative StressPhysical Conditioning, AnimalVentricular RemodelingAngiotensin IIAnimalsHypertensionInflammationMaleMyocardiumRatsRats, Inbred SHRRats, Inbred WKYReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionAngiotensin IIReactive Oxygen Species

Identifiers

PMID29232407
PMCPMC5726656
OpenAlexW2771795903

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.