MicroRNA in myogenesis and muscle atrophy
PURPOSE OF REVIEWTo understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation. RECENT FINDINGSMuscle wasting increases the risk of morbidity/mortality in primary muscle diseases, secondary muscle disorders and elderly popul...
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| Veröffentlicht in: | Current opinion in clinical nutrition and metabolic care 2013-05, Vol.16 (3), p.258-266 |
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| creator | Wang, Xiaonan H |
| description | PURPOSE OF REVIEWTo understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation.
RECENT FINDINGSMuscle 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.
SUMMARYGrowing 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. |
| doi_str_mv | 10.1097/MCO.0b013e32835f81b9 |
| format | Article |
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RECENT FINDINGSMuscle 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.
SUMMARYGrowing 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.</description><identifier>ISSN: 1363-1950</identifier><identifier>EISSN: 1473-6519</identifier><identifier>DOI: 10.1097/MCO.0b013e32835f81b9</identifier><identifier>PMID: 23449000</identifier><language>eng</language><publisher>England: Lippincott Williams & Wilkins, Inc</publisher><subject>Animals ; Cell Differentiation ; Cell Proliferation ; Disease Models, Animal ; Down-Regulation ; Humans ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Motor Activity ; Muscle Development - genetics ; Muscle Development - physiology ; Muscle Proteins - genetics ; Muscle Proteins - metabolism ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Muscular Atrophy - genetics ; Muscular Atrophy - metabolism ; Muscular Atrophy - pathology ; Myostatin - genetics ; Myostatin - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphoric Monoester Hydrolases - genetics ; Phosphoric Monoester Hydrolases - metabolism ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; Regeneration ; Signal Transduction ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Current opinion in clinical nutrition and metabolic care, 2013-05, Vol.16 (3), p.258-266</ispartof><rights>2013 Lippincott Williams & Wilkins, Inc.</rights><rights>2013 Wolters Kluwer Health | Lippincott Williams & Wilkins 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4579-d70714f9ee11fa9665cabab833002b39648b258f3906b5d50855e4ab24558b0c3</citedby><cites>FETCH-LOGICAL-c4579-d70714f9ee11fa9665cabab833002b39648b258f3906b5d50855e4ab24558b0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23449000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiaonan H</creatorcontrib><title>MicroRNA in myogenesis and muscle atrophy</title><title>Current opinion in clinical nutrition and metabolic care</title><addtitle>Curr Opin Clin Nutr Metab Care</addtitle><description>PURPOSE OF REVIEWTo understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation.
RECENT FINDINGSMuscle 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.
SUMMARYGrowing 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.</description><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Motor Activity</subject><subject>Muscle Development - genetics</subject><subject>Muscle Development - physiology</subject><subject>Muscle Proteins - genetics</subject><subject>Muscle Proteins - metabolism</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Muscular Atrophy - genetics</subject><subject>Muscular Atrophy - metabolism</subject><subject>Muscular Atrophy - pathology</subject><subject>Myostatin - genetics</subject><subject>Myostatin - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphoric Monoester Hydrolases - genetics</subject><subject>Phosphoric Monoester Hydrolases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Regeneration</subject><subject>Signal Transduction</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1363-1950</issn><issn>1473-6519</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKAzEUhoMoXqpvIDJLXUw9uc1MNoIUb6AWRNchmZ5pR-dSkxlL395Ia1EXrk7g_P-X5CPkmMKQgkrPH0bjIVigHDnLuCwyatUW2aci5XEiqdoOZ57wmCoJe-TA-1cAyhTwXbLHuBAKAPbJ2UOZu_bp8TIqm6hetlNs0Jc-Ms0kqnufVxiZzrXz2fKQ7BSm8ni0ngPycn31PLqN78c3d6PL-zgXMlXxJIWUikIhUloYlSQyN9bYjHMAZrlKRGaZzAquILFyIiGTEoWxTEiZWcj5gFysuPPe1jjJsemcqfTclbVxS92aUv_eNOVMT9sPHdhp-FgAnK4Brn3v0Xe6Ln2OVWUabHuvKWdJyhlTSYiKVTQ48N5hsbmGgv6yrINl_ddyqJ38fOKm9K01BLJVYNFWHTr_VvULdHqGpupm_7M_ATGZinw</recordid><startdate>201305</startdate><enddate>201305</enddate><creator>Wang, Xiaonan H</creator><general>Lippincott Williams & Wilkins, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201305</creationdate><title>MicroRNA in myogenesis and muscle atrophy</title><author>Wang, Xiaonan H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4579-d70714f9ee11fa9665cabab833002b39648b258f3906b5d50855e4ab24558b0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Humans</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Motor Activity</topic><topic>Muscle Development - genetics</topic><topic>Muscle Development - physiology</topic><topic>Muscle Proteins - genetics</topic><topic>Muscle Proteins - metabolism</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Muscular Atrophy - genetics</topic><topic>Muscular Atrophy - metabolism</topic><topic>Muscular Atrophy - pathology</topic><topic>Myostatin - genetics</topic><topic>Myostatin - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphoric Monoester Hydrolases - genetics</topic><topic>Phosphoric Monoester Hydrolases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Regeneration</topic><topic>Signal Transduction</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiaonan H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current opinion in clinical nutrition and metabolic care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiaonan H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA in myogenesis and muscle atrophy</atitle><jtitle>Current opinion in clinical nutrition and metabolic care</jtitle><addtitle>Curr Opin Clin Nutr Metab Care</addtitle><date>2013-05</date><risdate>2013</risdate><volume>16</volume><issue>3</issue><spage>258</spage><epage>266</epage><pages>258-266</pages><issn>1363-1950</issn><eissn>1473-6519</eissn><abstract>PURPOSE OF REVIEWTo understand the impact of microRNA on myogenesis and muscle wasting in order to provide valuable information for clinical investigation.
RECENT FINDINGSMuscle 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.
SUMMARYGrowing 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.</abstract><cop>England</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>23449000</pmid><doi>10.1097/MCO.0b013e32835f81b9</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Animals Cell Differentiation Cell Proliferation Disease Models, Animal Down-Regulation Humans Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - metabolism MicroRNAs - genetics MicroRNAs - metabolism Motor Activity Muscle Development - genetics Muscle Development - physiology Muscle Proteins - genetics Muscle Proteins - metabolism Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Muscular Atrophy - genetics Muscular Atrophy - metabolism Muscular Atrophy - pathology Myostatin - genetics Myostatin - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphoric Monoester Hydrolases - genetics Phosphoric Monoester Hydrolases - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism Regeneration Signal Transduction Transcription Factors - genetics Transcription Factors - metabolism |
| title | MicroRNA in myogenesis and muscle atrophy |
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