Evidence map›Paper›PMID 27305869›Full record

ArticleJournal of cellular and molecular medicine2016

Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats.

Luiz H M Bozi, Paulo R Jannig, Natale Rolim, Vanessa A Voltarelli, Paulo M M Dourado, Ulrik Wisløff, Patricia C Brum

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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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

7 authors at 2 institutions in 2 countries.

Luiz H M BoziSchool of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil.
Paulo R JannigSchool of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil.
Natale RolimK.G. Jebsen Center of Exercise in Medicine at Department of Circulation and Medical Imaging, Norwegian University of Science and Technology - NTNU, Trondheim, Norway.
Vanessa A VoltarelliSchool of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil.
Paulo M M DouradoDepartment of Pharmacology, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, Brazil.
Ulrik WisløffK.G. Jebsen Center of Exercise in Medicine at Department of Circulation and Medical Imaging, Norwegian University of Science and Technology - NTNU, Trondheim, Norway.
Patricia C BrumSchool of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil. pcbrum@usp.br.
Universidade de São Paulo · BRNorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac endoplasmic reticulum (ER) stress through accumulation of misfolded proteins plays a pivotal role in cardiovascular diseases. In an attempt to reestablish ER homoeostasis, the unfolded protein response (UPR) is activated. However, if ER stress persists, sustained UPR activation leads to apoptosis. There is no available therapy for ER stress relief. Considering that aerobic exercise training (AET) attenuates oxidative stress, mitochondrial dysfunction and calcium imbalance, it may be a potential strategy to reestablish cardiac ER homoeostasis. We test the hypothesis that AET would attenuate impaired cardiac ER stress after myocardial infarction (MI). Wistar rats underwent to either MI or sham surgeries. Four weeks later, rats underwent to 8 weeks of moderate-intensity AET. Myocardial infarction rats displayed cardiac dysfunction and lung oedema, suggesting heart failure. Cardiac dysfunction in MI rats was paralleled by increased protein levels of UPR markers (GRP78, DERLIN-1 and CHOP), accumulation of misfolded and polyubiquitinated proteins, and reduced chymotrypsin-like proteasome activity. These results suggest an impaired cardiac protein quality control. Aerobic exercise training improved exercise capacity and cardiac function of MI animals. Interestingly, AET blunted MI-induced ER stress by reducing protein levels of UPR markers, and accumulation of both misfolded and polyubiquinated proteins, which was associated with restored proteasome activity. Taken together, our study provide evidence for AET attenuation of ER stress through the reestablishment of cardiac protein quality control, which contributes to better cardiac function in post-MI heart failure rats. These results reinforce the importance of AET as primary non-pharmacological therapy to cardiovascular disease.

Indexed as

Endoplasmic Reticulum StressPhysical Conditioning, AnimalAnimalsHeart FailureHeart Function TestsMyocardial InfarctionMyocardiumProtein FoldingProteinsRats, WistarProteinsendoplasmic reticulum stressexercisemyocardial infarctionprotein quality control

Identifiers

PMID27305869
PMCPMC5082404
OpenAlexW2432832697

What OpenQuestion holds

Textmetadata
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.