Document Detail

MicroRNA in myogenesis and muscle atrophy.
MedLine Citation:
PMID:  23449000     Owner:  NLM     Status:  MEDLINE    
PURPOSE OF REVIEW: To understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation.
RECENT FINDINGS: Muscle wasting increases the risk of morbidity/mortality in primary muscle diseases, secondary muscle disorders and elderly population. Muscle mass is controlled by several different signalling pathways. Insulin-like growth factor/PI3K/Akt is a positive signalling pathway, as it increases muscle mass by increasing protein synthesis and decreasing protein degradation. This pathway is directly and/or indirectly downregulated by miR-1, miR-133, miR-206 or miR-125b, and upregulated by miR-23a or miR-486. Myostatin and the transforming growth factor-β signalling pathway are negative regulators that cause muscle wasting. An increase of miR-27 reduces myostatin and increases muscle cell proliferation. Muscle regeneration capacity also plays a significant role in the regulation of muscle mass. This review comprehensively describes the effect of microRNA on myoblasts proliferation and differentiation, and summarizes the varied influences of microRNA on different muscle atrophy.
SUMMARY: Growing evidence indicates that microRNAs significantly impact muscle growth, regeneration and metabolism. MicroRNAs have a great potential to become diagnostic and/or prognostic markers, therapeutic agents and therapeutic targets.
Xiaonan H Wang
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current opinion in clinical nutrition and metabolic care     Volume:  16     ISSN:  1473-6519     ISO Abbreviation:  Curr Opin Clin Nutr Metab Care     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-04-11     Completed Date:  2013-12-10     Revised Date:  2014-03-31    
Medline Journal Info:
Nlm Unique ID:  9804399     Medline TA:  Curr Opin Clin Nutr Metab Care     Country:  England    
Other Details:
Languages:  eng     Pagination:  258-66     Citation Subset:  IM    
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MeSH Terms
Cell Differentiation
Cell Proliferation
Disease Models, Animal
Insulin-Like Growth Factor I / genetics,  metabolism
MicroRNAs / genetics,  metabolism*
Motor Activity
Muscle Development / genetics,  physiology*
Muscle Proteins / genetics,  metabolism
Muscle, Skeletal / metabolism,  pathology
Muscular Atrophy / genetics,  metabolism,  pathology*
Myostatin / genetics,  metabolism
PTEN Phosphohydrolase / genetics,  metabolism
Phosphatidylinositol 3-Kinases / genetics,  metabolism
Phosphoric Monoester Hydrolases / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism
Signal Transduction
Transcription Factors / genetics,  metabolism
Grant Support
Reg. No./Substance:
0/MicroRNAs; 0/Muscle Proteins; 0/Myostatin; 0/PPARGC1A protein, human; 0/Transcription Factors; 67763-96-6/Insulin-Like Growth Factor I; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC Proteins c-akt; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC Phosphohydrolase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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