Evidence map›Paper›PMID 25954323›Full record

ArticleOxidative medicine and cellular longevity2015

Increased clearance of reactive aldehydes and damaged proteins in hypertension-induced compensated cardiac hypertrophy: impact of exercise training.

Juliane Cruz Campos, Tiago Fernandes, Luiz Roberto Grassmann Bechara, Nathalie Alves da Paixão, Patricia Chakur Brum, Edilamar Menezes de Oliveira, Julio Cesar Batista Ferreira

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

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.4field-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

23 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Impacts of exercise intervention on various diseases in rats.Journal of sport and health science · 2020
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Cardiac basal autophagic activity and increased exercise capacity.The journal of physiological sciences : JPS · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Juliane Cruz CamposDepartment of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, 05508-000 Sao Paulo, SP, Brazil.
Tiago FernandesSchool of Physical Education and Sport, University of Sao Paulo, 05508-030 Sao Paulo, SP, Brazil.
Luiz Roberto Grassmann BecharaDepartment of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, 05508-000 Sao Paulo, SP, Brazil.
Nathalie Alves da PaixãoSchool of Physical Education and Sport, University of Sao Paulo, 05508-030 Sao Paulo, SP, Brazil.
Patricia Chakur BrumSchool of Physical Education and Sport, University of Sao Paulo, 05508-030 Sao Paulo, SP, Brazil.
Edilamar Menezes de OliveiraSchool of Physical Education and Sport, University of Sao Paulo, 05508-030 Sao Paulo, SP, Brazil.
Julio Cesar Batista FerreiraDepartment of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, 05508-000 Sao Paulo, SP, Brazil.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe previously reported that exercise training (ET) facilitates the clearance of damaged proteins in heart failure. Here, we characterized the impact of ET on cardiac protein quality control during compensated ventricular hypertrophy in spontaneously hypertensive rats (SHR). METHODS AND

resultsSHR were randomly assigned into sedentary and swimming-trained groups. Sedentary SHR displayed cardiac hypertrophy with preserved ventricular function compared to normotensive rats, characterizing a compensated cardiac hypertrophy. Hypertensive rats presented signs of cardiac oxidative stress, depicted by increased lipid peroxidation. However, these changes were not followed by accumulation of lipid peroxidation-generated reactive aldehydes and damaged proteins. This scenario was explained, at least in part, by the increased catalytic activity of both aldehyde dehydrogenase 2 (ALDH2) and proteasome. Of interest, ET exacerbated cardiac hypertrophy, improved ventricular function, induced resting bradycardia, and decreased blood pressure in SHR. These changes were accompanied by reduced cardiac oxidative stress and a consequent decrease in ALDH2 and proteasome activities, without affecting small chaperones levels and apoptosis in SHR.

conclusionIncreased cardiac ALDH2 and proteasomal activities counteract the deleterious effect of excessive oxidative stress in hypertension-induced compensated cardiac hypertrophy in rats. ET has a positive effect in reducing cardiac oxidative stress without affecting protein quality control.

Indexed as

Aldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAldehydesAnimalsBlood PressureCardiomegalyHeart RateHypertensionLipid PeroxidationMaleMitochondrial ProteinsPhysical Conditioning, AnimalProteasome Endopeptidase ComplexProtein CarbonylationRatsRats, Inbred SHRAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAldehydesAldh2 protein, ratMitochondrial ProteinsProteasome Endopeptidase Complex

Identifiers

PMID25954323
PMCPMC4411445
OpenAlexW2047937770

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.