Evidence map›Paper›PMID 34439993›Full record

ArticleBiology2021

Identification of Potentially Related Genes and Mechanisms Involved in Skeletal Muscle Atrophy Induced by Excessive Exercise in Zebrafish.

Chen-Chen Sun, Zuo-Qiong Zhou, Zhang-Lin Chen, Run-Kang Zhu, Dong Yang, Xi-Yang Peng, Lan Zheng, Chang-Fa Tang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

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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

6 citing papers in PubMed.

  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

8 authors.

Chen-Chen SunKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Zuo-Qiong ZhouKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Zhang-Lin ChenKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Run-Kang ZhuKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Dong YangKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Xi-Yang PengKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Lan ZhengKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.
Chang-Fa TangKey Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha 410012, China.

Funding

Hunan Provincial Natural Science Foundation of China 2020JJ5354National Natural Science Foundation of China 81801392 , 32071175Postgraduate Scientific Research Innovation Project of Hunan Province CX20200532
6 · The paper itself

Abstract

Long-term imbalance between fatigue and recovery may eventually lead to muscle weakness or even atrophy. We previously reported that excessive exercise induces pathological cardiac hypertrophy. However, the effect of excessive exercise on the skeletal muscles remains unclear. In the present study, we successfully established an excessive-exercise-induced skeletal muscle atrophy zebrafish model, with decreased muscle fiber size, critical swimming speed, and maximal oxygen consumption. High-throughput RNA-seq analysis identified differentially expressed genes in the model system compared with control zebrafish. Gene ontology and KEGG enrichment analysis revealed that the upregulated genes were enriched in autophagy, homeostasis, circadian rhythm, response to oxidative stress, apoptosis, the p53 signaling pathway, and the FoxO signaling pathway. Protein-protein interaction network analysis identified several hub genes, including keap1b, per3, ulk1b, socs2, esrp1, bcl2l1, hsp70, igf2r, mdm2, rab18a, col1a1a, fn1a, ppih, tpx2, uba5, nhlrc2, mcm4, tac1, b3gat3, and ddost, that correlate with the pathogenesis of skeletal muscle atrophy induced by excessive exercise. The underlying regulatory pathways and muscle-pressure-response-related genes identified in the present study will provide valuable insights for prescribing safe and accurate exercise programs for athletes and the supervision and clinical treatment of muscle atrophy induced by excessive exercise.

Indexed as

excessive exerciseFoxO signaling pathwayp53 signaling pathwayskeletal muscle atrophyWnt signaling pathway

Identifiers

PMID34439993
PMCPMC8389602

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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.