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Bioinformatics Analysis Reveals MicroRNAs Regulating Biological Pathways in Exercise-Induced Cardiac Physiological Hypertrophy.

Abstract Exercise-induced physiological cardiac hypertrophy is generally considered to be a type of adaptive change after exercise training and is beneficial for cardiovascular diseases. This study aims at investigating exercise-regulated microRNAs (miRNAs) and their potential biological pathways. Here, we collected 23 miRNAs from 8 published studies. MirPath v.3 from the DIANA tools website was used to execute the analysis, and TargetScan was used to predict the target genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to identify potential pathways and functional annotations associated with exercise-induced physiological cardiac hypertrophy. Various miRNA targets and molecular pathways, such as Fatty acid elongation, Arrhythmogenic right ventricular cardiomyopathy (ARVC), and ECM-receptor interaction, were identified. This study could prompt the understanding of the regulatory mechanisms underlying exercise-induced physiological cardiac hypertrophy.
PMID
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Authors

Mayor MeshTerms

Cardiomegaly, Exercise-Induced

Computational Biology

Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28286759
OWN - NLM
STAT- MEDLINE
DA  - 20170313
DCOM- 20170317
LR  - 20170317
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Bioinformatics Analysis Reveals MicroRNAs Regulating Biological Pathways in
      Exercise-Induced Cardiac Physiological Hypertrophy.
PG  - 2850659
LID - 10.1155/2017/2850659 [doi]
AB  - Exercise-induced physiological cardiac hypertrophy is generally considered to be 
      a type of adaptive change after exercise training and is beneficial for
      cardiovascular diseases. This study aims at investigating exercise-regulated
      microRNAs (miRNAs) and their potential biological pathways. Here, we collected 23
      miRNAs from 8 published studies. MirPath v.3 from the DIANA tools website was
      used to execute the analysis, and TargetScan was used to predict the target
      genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO)
      analyses were performed to identify potential pathways and functional annotations
      associated with exercise-induced physiological cardiac hypertrophy. Various miRNA
      targets and molecular pathways, such as Fatty acid elongation, Arrhythmogenic
      right ventricular cardiomyopathy (ARVC), and ECM-receptor interaction, were
      identified. This study could prompt the understanding of the regulatory
      mechanisms underlying exercise-induced physiological cardiac hypertrophy.
FAU - Xu, Jiahong
AU  - Xu J
AD  - Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, 
      Shanghai 200065, China.
FAU - Liu, Yang
AU  - Liu Y
AD  - Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, 
      Shanghai 200065, China.
FAU - Xie, Yuan
AU  - Xie Y
AD  - Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, 
      Shanghai 200065, China.
FAU - Zhao, Cuimei
AU  - Zhao C
AUID- ORCID: 0000-0001-6239-498X
AD  - Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, 
      Shanghai 200065, China.
FAU - Wang, Hongbao
AU  - Wang H
AUID- ORCID: 0000-0002-1103-3292
AD  - Department of Cardiology, Yangpu Hospital, Tongji University School of Medicine, 
      Shanghai 200090, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170214
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Arrhythmogenic Right Ventricular Dysplasia/genetics/*metabolism/physiopathology
MH  - *Cardiomegaly, Exercise-Induced
MH  - *Computational Biology
MH  - Humans
MH  - MicroRNAs/*metabolism
PMC - PMC5329648
COI - The authors declare that there are no competing interests.
EDAT- 2017/03/14 06:00
MHDA- 2017/03/18 06:00
CRDT- 2017/03/14 06:00
PHST- 2016/09/30 [received]
PHST- 2016/12/20 [accepted]
AID - 10.1155/2017/2850659 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:2850659. doi: 10.1155/2017/2850659. Epub 2017 Feb 14.

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