Evidence map›Paper›PMID 25874020›Full record

ArticleOxidative medicine and cellular longevity2015

Acute exercise induced mitochondrial H₂O₂ production in mouse skeletal muscle: association with p(66Shc) and FOXO3a signaling and antioxidant enzymes.

Ping Wang, Chun Guang Li, Zhengtang Qi, Di Cui, Shuzhe Ding

Open access · hybridAbstract read
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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

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  17. Autophagy-Dependent Beneficial Effects of Exercise.Cold Spring Harbor perspectives in medicine · 2017
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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

5 authors at 3 institutions in 2 countries.

Ping WangSchool of Physical Education and Sports Science, Hangzhou Normal University, Hangzhou 311121, China.
Chun Guang LiNational Institute of Complementary Medicine, University of Western Sydney, Penrith, NSW 2751, Australia.ORCID 0000-0002-7789-2209
Zhengtang QiKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
Di CuiKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China.
Shuzhe DingKey Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China ; College of Physical Education and Health, East China Normal University, Shanghai 200241, China.
East China Normal University · CNHangzhou Normal University · CNWestern Sydney University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise induced skeletal muscle phenotype change involves a complex interplay between signaling pathways and downstream regulators. This study aims to investigate the effect of acute exercise on mitochondrial H2O2 production and its association with p(66Shc), FOXO3a, and antioxidant enzymes. Male ICR/CD-1 mice were subjected to an acute exercise. Muscle tissues (gastrocnemius and quadriceps femoris) were taken after exercise to measure mitochondrial H2O2 content, expression of p(66Shc) and FOXO3a, and the activity of antioxidant enzymes. The results showed that acute exercise significantly increased mitochondrial H2O2 content and expressions of p(66Shc) and FOXO3a in a time-dependent manner, with a linear correlation between the increase in H2O2 content and p(66Shc) or FOXO3a expression. The activity of mitochondrial catalase was slightly reduced in the 90 min exercise group, but it was significantly higher in groups with 120 and 150 min exercise compared to that of 90 min exercise group. The activity of SOD was not significantly affected. The results indicate that acute exercise increases mitochondrial H2O2 production in the skeletal muscle, which is associated with the upregulation of p(66Shc) and FOXO3a. The association of p(66Shc) and FOXO3a signaling with exercise induced H2O2 generation may play a role in regulating cellular oxidative stress during acute exercise.

Indexed as

AnimalsAntioxidantsCatalaseForkhead Box Protein O3Forkhead Transcription FactorsHydrogen PeroxideMaleMiceMice, Inbred ICRMitochondriaMuscle, SkeletalOxidative StressPhysical Conditioning, AnimalRNA, MessengerShc Signaling Adaptor ProteinsSignal TransductionAntioxidantsCatalaseForkhead Box Protein O3Forkhead Transcription FactorsFoxO3 protein, mouseHydrogen PeroxideRNA, MessengerShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Superoxide Dismutase

Identifiers

PMID25874020
PMCPMC4385701
OpenAlexW1991478054

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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.