Role of PGC-1α signaling in skeletal muscle health and disease
This paper reviews the current understanding of the molecular basis of the peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α)–mediated pathway and discusses the role of PGC‐1α in skeletal muscle atrophy caused by immobilization. PGC‐1α is the master transcription regulator that sti...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2012-10, Vol.1271 (1), p.110-117 |
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| creator | Kang, Chounghun Li Ji, Li |
| description | This paper reviews the current understanding of the molecular basis of the peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α)–mediated pathway and discusses the role of PGC‐1α in skeletal muscle atrophy caused by immobilization. PGC‐1α is the master transcription regulator that stimulates mitochondrial biogenesis, by upregulating nuclear respiratory factors (NRF‐1, 2) and mitochondrial transcription factor A (Tfam), which leads to increased mitochondrial DNA replication and gene transcription. PGC‐1α also regulates cellular oxidant–antioxidant homeostasis by stimulating the gene expression of superoxide dismutase‐2 (SOD2), catalase, glutathione peroxidase 1 (GPx1), and uncoupling protein (UCP). Recent reports from muscle‐specific PGC‐1α overexpression underline the importance of PGC‐1α in atrophied skeletal muscle, demonstrate enhancement of the PGC‐1α mitochondrial biogenic pathway, and reduced oxidative damage. Thus, PGC‐1α appears to play a protective role against atrophy‐linked skeletal muscle deterioration. |
| doi_str_mv | 10.1111/j.1749-6632.2012.06738.x |
| format | Article |
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PGC‐1α is the master transcription regulator that stimulates mitochondrial biogenesis, by upregulating nuclear respiratory factors (NRF‐1, 2) and mitochondrial transcription factor A (Tfam), which leads to increased mitochondrial DNA replication and gene transcription. PGC‐1α also regulates cellular oxidant–antioxidant homeostasis by stimulating the gene expression of superoxide dismutase‐2 (SOD2), catalase, glutathione peroxidase 1 (GPx1), and uncoupling protein (UCP). Recent reports from muscle‐specific PGC‐1α overexpression underline the importance of PGC‐1α in atrophied skeletal muscle, demonstrate enhancement of the PGC‐1α mitochondrial biogenic pathway, and reduced oxidative damage. Thus, PGC‐1α appears to play a protective role against atrophy‐linked skeletal muscle deterioration.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/j.1749-6632.2012.06738.x</identifier><identifier>PMID: 23050972</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Aging - metabolism ; Animals ; Atrophy ; Catalase ; Cellular ; Exercise ; Gene expression ; Gene Expression Regulation, Enzymologic ; Heat-Shock Proteins - biosynthesis ; Heat-Shock Proteins - metabolism ; Homeostasis ; Humans ; inflammation ; mitochondria ; Mitochondrial Turnover ; muscle atrophy ; Muscle, Skeletal - immunology ; Muscle, Skeletal - metabolism ; Muscles ; Muscular Atrophy - metabolism ; Musculoskeletal Diseases - immunology ; Musculoskeletal Diseases - metabolism ; Original ; Oxidoreductases - biosynthesis ; Oxidoreductases - genetics ; Oxidoreductases - metabolism ; Pathways ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; PGC-1 ; Protective ; Signal Transduction ; Transcription Factors - biosynthesis ; Transcription Factors - metabolism</subject><ispartof>Annals of the New York Academy of Sciences, 2012-10, Vol.1271 (1), p.110-117</ispartof><rights>2012 New York Academy of Sciences.</rights><rights>2012 New York Academy of Sciences. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5798-d0e077293cc575ad08cbf8eb6ed54dc55c26e271c7d250b2c10fd5d9837e193c3</citedby><cites>FETCH-LOGICAL-c5798-d0e077293cc575ad08cbf8eb6ed54dc55c26e271c7d250b2c10fd5d9837e193c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1749-6632.2012.06738.x$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1749-6632.2012.06738.x$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23050972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kang, Chounghun</creatorcontrib><creatorcontrib>Li Ji, Li</creatorcontrib><title>Role of PGC-1α signaling in skeletal muscle health and disease</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>This paper reviews the current understanding of the molecular basis of the peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α)–mediated pathway and discusses the role of PGC‐1α in skeletal muscle atrophy caused by immobilization. PGC‐1α is the master transcription regulator that stimulates mitochondrial biogenesis, by upregulating nuclear respiratory factors (NRF‐1, 2) and mitochondrial transcription factor A (Tfam), which leads to increased mitochondrial DNA replication and gene transcription. PGC‐1α also regulates cellular oxidant–antioxidant homeostasis by stimulating the gene expression of superoxide dismutase‐2 (SOD2), catalase, glutathione peroxidase 1 (GPx1), and uncoupling protein (UCP). Recent reports from muscle‐specific PGC‐1α overexpression underline the importance of PGC‐1α in atrophied skeletal muscle, demonstrate enhancement of the PGC‐1α mitochondrial biogenic pathway, and reduced oxidative damage. Thus, PGC‐1α appears to play a protective role against atrophy‐linked skeletal muscle deterioration.</description><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Atrophy</subject><subject>Catalase</subject><subject>Cellular</subject><subject>Exercise</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Heat-Shock Proteins - biosynthesis</subject><subject>Heat-Shock Proteins - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>inflammation</subject><subject>mitochondria</subject><subject>Mitochondrial Turnover</subject><subject>muscle atrophy</subject><subject>Muscle, Skeletal - immunology</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscles</subject><subject>Muscular Atrophy - metabolism</subject><subject>Musculoskeletal Diseases - immunology</subject><subject>Musculoskeletal Diseases - metabolism</subject><subject>Original</subject><subject>Oxidoreductases - biosynthesis</subject><subject>Oxidoreductases - genetics</subject><subject>Oxidoreductases - metabolism</subject><subject>Pathways</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>PGC-1</subject><subject>Protective</subject><subject>Signal Transduction</subject><subject>Transcription Factors - biosynthesis</subject><subject>Transcription Factors - metabolism</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNqNkc1uEzEUhS0EoqHwCshLNjP1z3hsb0BVRFNo1VYFhFhZjn0ncerMlPGkpI_Fi_BMOE0bYFXuxrbOd4-u70EIU1LSXAeLkspKF3XNWckIZSWpJVfl-gka7YSnaESIlIXSjO-hFyktSCZVJZ-jPcaJIFqyEXp32UXAXYMvJuOC_vqJU5i1NoZ2hkOL0xVEGGzEy1VymZuDjcMc29ZjHxLYBC_Rs8bGBK_uz3305ej95_FxcXo--TA-PC2ckFoVnkCehWnu8ltYT5SbNgqmNXhReSeEYzUwSZ30TJApc5Q0XnituASau_g-erv1vV5Nl-AdtENvo7nuw9L2t6azwfyrtGFuZt2N4ZXWtVDZ4M29Qd99X0EazDIkBzHaFrpVMlSRvBPGK_44KhURtFJUPo7mUqIWWmRUbVHXdyn10OyGp-SOMwuzCc9swjObVM1dqmadW1___fld40OMf7bzI0S4_W9jc_bt8NPmmg2KrUFIA6x3Bra_MlmXwnw9m5hLdXLBTz7WRvDfTrS_fw</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Kang, Chounghun</creator><creator>Li Ji, Li</creator><general>Blackwell Publishing Inc</general><scope>BSCLL</scope><scope>24P</scope><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>7ST</scope><scope>C1K</scope><scope>SOI</scope><scope>7SP</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope><scope>5PM</scope></search><sort><creationdate>201210</creationdate><title>Role of PGC-1α signaling in skeletal muscle health and disease</title><author>Kang, Chounghun ; Li Ji, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5798-d0e077293cc575ad08cbf8eb6ed54dc55c26e271c7d250b2c10fd5d9837e193c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Atrophy</topic><topic>Catalase</topic><topic>Cellular</topic><topic>Exercise</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Heat-Shock Proteins - biosynthesis</topic><topic>Heat-Shock Proteins - metabolism</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>inflammation</topic><topic>mitochondria</topic><topic>Mitochondrial Turnover</topic><topic>muscle atrophy</topic><topic>Muscle, Skeletal - immunology</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscles</topic><topic>Muscular Atrophy - metabolism</topic><topic>Musculoskeletal Diseases - immunology</topic><topic>Musculoskeletal Diseases - metabolism</topic><topic>Original</topic><topic>Oxidoreductases - biosynthesis</topic><topic>Oxidoreductases - genetics</topic><topic>Oxidoreductases - metabolism</topic><topic>Pathways</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>PGC-1</topic><topic>Protective</topic><topic>Signal Transduction</topic><topic>Transcription Factors - biosynthesis</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kang, Chounghun</creatorcontrib><creatorcontrib>Li Ji, Li</creatorcontrib><collection>Istex</collection><collection>Wiley-Blackwell Open Access Collection</collection><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>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kang, Chounghun</au><au>Li Ji, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of PGC-1α signaling in skeletal muscle health and disease</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2012-10</date><risdate>2012</risdate><volume>1271</volume><issue>1</issue><spage>110</spage><epage>117</epage><pages>110-117</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>This paper reviews the current understanding of the molecular basis of the peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α)–mediated pathway and discusses the role of PGC‐1α in skeletal muscle atrophy caused by immobilization. PGC‐1α is the master transcription regulator that stimulates mitochondrial biogenesis, by upregulating nuclear respiratory factors (NRF‐1, 2) and mitochondrial transcription factor A (Tfam), which leads to increased mitochondrial DNA replication and gene transcription. PGC‐1α also regulates cellular oxidant–antioxidant homeostasis by stimulating the gene expression of superoxide dismutase‐2 (SOD2), catalase, glutathione peroxidase 1 (GPx1), and uncoupling protein (UCP). Recent reports from muscle‐specific PGC‐1α overexpression underline the importance of PGC‐1α in atrophied skeletal muscle, demonstrate enhancement of the PGC‐1α mitochondrial biogenic pathway, and reduced oxidative damage. Thus, PGC‐1α appears to play a protective role against atrophy‐linked skeletal muscle deterioration.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>23050972</pmid><doi>10.1111/j.1749-6632.2012.06738.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging - metabolism Animals Atrophy Catalase Cellular Exercise Gene expression Gene Expression Regulation, Enzymologic Heat-Shock Proteins - biosynthesis Heat-Shock Proteins - metabolism Homeostasis Humans inflammation mitochondria Mitochondrial Turnover muscle atrophy Muscle, Skeletal - immunology Muscle, Skeletal - metabolism Muscles Muscular Atrophy - metabolism Musculoskeletal Diseases - immunology Musculoskeletal Diseases - metabolism Original Oxidoreductases - biosynthesis Oxidoreductases - genetics Oxidoreductases - metabolism Pathways Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha PGC-1 Protective Signal Transduction Transcription Factors - biosynthesis Transcription Factors - metabolism |
| title | Role of PGC-1α signaling in skeletal muscle health and disease |
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