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TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia
Background Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating a...
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| Published in: | Journal of cachexia, sarcopenia and muscle sarcopenia and muscle, 2024-10, Vol.15 (5), p.2056-2070 |
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| container_title | Journal of cachexia, sarcopenia and muscle |
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| creator | Guo, Ai Huang, Ke Lu, Quanyi Tao, Bailong Li, Kai Jiang, Dianming |
| description | Background
Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating antioxidant responses to mitigate oxidative stress, yet its regulatory role in skeletal muscle remains unclear. This study aims to elucidate the impact of TRIM16 on enhancing antioxidant response through SIRT‐1, consequently mitigating age‐related oxidative stress, and ameliorating muscle atrophy.
Methods
Aged mouse models were established utilizing male mice at 18 months with D‐galactose (D‐gal, 200 mg/kg) intervention and at 24 months with natural aging, while 3‐month‐old young mice served as controls. Muscle cell senescence was induced in C2C12 myoblasts using 30 g/L D‐gal. TRIM16 was overexpressed in the skeletal muscle of aged mice and silenced/overexpressed in C2C12 myoblasts. The effects of TRIM16 on skeletal muscle mass, grip strength, morphological changes, myotube formation, myogenic differentiation, and muscle atrophy indicators were evaluated. Reactive oxygen species (ROS) levels and oxidative stress‐related parameters were measured. The SIRT‐1 inhibitor EX‐527 was employed to elucidate the protective role of TRIM16 mediated through SIRT‐1.
Results
Aged mice displayed significant reductions in lean mass (−11.58%; −14.47% vs. young, P |
| doi_str_mv | 10.1002/jcsm.13553 |
| format | article |
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Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating antioxidant responses to mitigate oxidative stress, yet its regulatory role in skeletal muscle remains unclear. This study aims to elucidate the impact of TRIM16 on enhancing antioxidant response through SIRT‐1, consequently mitigating age‐related oxidative stress, and ameliorating muscle atrophy.
Methods
Aged mouse models were established utilizing male mice at 18 months with D‐galactose (D‐gal, 200 mg/kg) intervention and at 24 months with natural aging, while 3‐month‐old young mice served as controls. Muscle cell senescence was induced in C2C12 myoblasts using 30 g/L D‐gal. TRIM16 was overexpressed in the skeletal muscle of aged mice and silenced/overexpressed in C2C12 myoblasts. The effects of TRIM16 on skeletal muscle mass, grip strength, morphological changes, myotube formation, myogenic differentiation, and muscle atrophy indicators were evaluated. Reactive oxygen species (ROS) levels and oxidative stress‐related parameters were measured. The SIRT‐1 inhibitor EX‐527 was employed to elucidate the protective role of TRIM16 mediated through SIRT‐1.
Results
Aged mice displayed significant reductions in lean mass (−11.58%; −14.47% vs. young, P < 0.05), hindlimb lean mass (−17.38%; −15.95% vs. young, P < 0.05), and grip strength (−22.29%; −31.45% vs. young, P < 0.01). Skeletal muscle fibre cross‐sectional area (CSA) decreased (−29.30%; −24.12% vs. young, P < 0.05). TRIM16 expression significantly decreased in aging skeletal muscle (−56.82%; −66.27% vs. young, P < 0.001) and senescent muscle cells (−46.53% vs. control, P < 0.001). ROS levels increased (+69.83% vs. control, P < 0.001), and myotube formation decreased in senescent muscle cells (−56.68% vs. control, P < 0.001). Expression of myogenic differentiation and antioxidant indicators decreased, while muscle atrophy markers increased in vivo and in vitro (all P < 0.05). Silencing TRIM16 in myoblasts induced oxidative stress and myotube atrophy, while TRIM16 overexpression partially mitigated aging effects on skeletal muscle. TRIM16 activation enhanced SIRT‐1 expression (+75.38% vs. control, P < 0.001). SIRT‐1 inhibitor EX‐527 (100 μM) suppressed TRIM16's antioxidant response and mitigating muscle atrophy, offsetting the protective effect of TRIM16 on senescent muscle cells.
Conclusions
This study elucidates TRIM16's role in mitigating oxidative stress and ameliorating muscle atrophy through the activation of SIRT‐1‐dependent antioxidant effects. TRIM16 emerges as a potential therapeutic target for age‐related sarcopenia.]]></description><identifier>ISSN: 2190-5991</identifier><identifier>ISSN: 2190-6009</identifier><identifier>EISSN: 2190-6009</identifier><identifier>DOI: 10.1002/jcsm.13553</identifier><identifier>PMID: 39192479</identifier><language>eng</language><publisher>Germany: John Wiley & Sons, Inc</publisher><subject>Antibodies ; Antioxidants ; Biotechnology ; Body composition ; Cell growth ; Homeostasis ; Laboratory animals ; Medical research ; Microscopy ; Muscle atrophy ; Musculoskeletal system ; Nitric oxide ; Original ; Oxidative stress ; Penicillin ; Proteins ; Reactive oxygen species ; Sarcopenia ; Senescence ; TRIM16</subject><ispartof>Journal of cachexia, sarcopenia and muscle, 2024-10, Vol.15 (5), p.2056-2070</ispartof><rights>2024 The Author(s). Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4043-d8b5b374afeeffd49511383c6a25259a95775cbf2e7a1d5a065505234aa87ccd3</cites><orcidid>0000-0001-9935-7066</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3112226846/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3112226846?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,25753,27924,27925,37012,37013,44590,46052,46476,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39192479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Ai</creatorcontrib><creatorcontrib>Huang, Ke</creatorcontrib><creatorcontrib>Lu, Quanyi</creatorcontrib><creatorcontrib>Tao, Bailong</creatorcontrib><creatorcontrib>Li, Kai</creatorcontrib><creatorcontrib>Jiang, Dianming</creatorcontrib><title>TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia</title><title>Journal of cachexia, sarcopenia and muscle</title><addtitle>J Cachexia Sarcopenia Muscle</addtitle><description><![CDATA[Background
Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating antioxidant responses to mitigate oxidative stress, yet its regulatory role in skeletal muscle remains unclear. This study aims to elucidate the impact of TRIM16 on enhancing antioxidant response through SIRT‐1, consequently mitigating age‐related oxidative stress, and ameliorating muscle atrophy.
Methods
Aged mouse models were established utilizing male mice at 18 months with D‐galactose (D‐gal, 200 mg/kg) intervention and at 24 months with natural aging, while 3‐month‐old young mice served as controls. Muscle cell senescence was induced in C2C12 myoblasts using 30 g/L D‐gal. TRIM16 was overexpressed in the skeletal muscle of aged mice and silenced/overexpressed in C2C12 myoblasts. The effects of TRIM16 on skeletal muscle mass, grip strength, morphological changes, myotube formation, myogenic differentiation, and muscle atrophy indicators were evaluated. Reactive oxygen species (ROS) levels and oxidative stress‐related parameters were measured. The SIRT‐1 inhibitor EX‐527 was employed to elucidate the protective role of TRIM16 mediated through SIRT‐1.
Results
Aged mice displayed significant reductions in lean mass (−11.58%; −14.47% vs. young, P < 0.05), hindlimb lean mass (−17.38%; −15.95% vs. young, P < 0.05), and grip strength (−22.29%; −31.45% vs. young, P < 0.01). Skeletal muscle fibre cross‐sectional area (CSA) decreased (−29.30%; −24.12% vs. young, P < 0.05). TRIM16 expression significantly decreased in aging skeletal muscle (−56.82%; −66.27% vs. young, P < 0.001) and senescent muscle cells (−46.53% vs. control, P < 0.001). ROS levels increased (+69.83% vs. control, P < 0.001), and myotube formation decreased in senescent muscle cells (−56.68% vs. control, P < 0.001). Expression of myogenic differentiation and antioxidant indicators decreased, while muscle atrophy markers increased in vivo and in vitro (all P < 0.05). Silencing TRIM16 in myoblasts induced oxidative stress and myotube atrophy, while TRIM16 overexpression partially mitigated aging effects on skeletal muscle. TRIM16 activation enhanced SIRT‐1 expression (+75.38% vs. control, P < 0.001). SIRT‐1 inhibitor EX‐527 (100 μM) suppressed TRIM16's antioxidant response and mitigating muscle atrophy, offsetting the protective effect of TRIM16 on senescent muscle cells.
Conclusions
This study elucidates TRIM16's role in mitigating oxidative stress and ameliorating muscle atrophy through the activation of SIRT‐1‐dependent antioxidant effects. TRIM16 emerges as a potential therapeutic target for age‐related sarcopenia.]]></description><subject>Antibodies</subject><subject>Antioxidants</subject><subject>Biotechnology</subject><subject>Body composition</subject><subject>Cell growth</subject><subject>Homeostasis</subject><subject>Laboratory animals</subject><subject>Medical research</subject><subject>Microscopy</subject><subject>Muscle atrophy</subject><subject>Musculoskeletal system</subject><subject>Nitric oxide</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Penicillin</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Sarcopenia</subject><subject>Senescence</subject><subject>TRIM16</subject><issn>2190-5991</issn><issn>2190-6009</issn><issn>2190-6009</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kl9rFDEQwBdRbKl98QPIgi8iXM3kz-7mSeSwetIitOdzmE1mzxx7mzPZq_atH8HP6Ccx98difTAQMmR-82MYpiieAzsDxvibpU2rMxBKiUfFMQfNJhVj-vEhVlrDUXGa0pLlIyuoFHtaHAkNmstaHxfr-dXsEqqyQ-t7P-JIqbyeXc1_3f2EfB2taXA0jGWkxabH0YehDF2JQ45-eIe7TFqHIVE5hhL7nm58tpS4oFwfKdeQKxNGG7LK47PiSYd9otPDe1J8OX8_n36cXHz-MJu-u5hYyaSYuKZVragldkRd56RWAKIRtkKuuNKoVV0r23acagSnkFVKMcWFRGxqa504KWZ7rwu4NOvoVxhvTUBvdh8hLgzG0duejNYOWq2EELaVnW41WlZJ0YDsuOYty663e9d6067I2TyPiP0D6cPM4L-aRbgxAFJWNdsaXh0MMXzbUBrNyidLfY8DhU0ygum6UQIYZPTlP-gybOKQZ2UEAOe8amSVqdd7ysaQUqTuvhtgZrsYZrsYZrcYGX7xd__36J81yADsge--p9v_qMyn6fXlXvob3pHGRw</recordid><startdate>202410</startdate><enddate>202410</enddate><creator>Guo, Ai</creator><creator>Huang, Ke</creator><creator>Lu, Quanyi</creator><creator>Tao, Bailong</creator><creator>Li, Kai</creator><creator>Jiang, Dianming</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-9935-7066</orcidid></search><sort><creationdate>202410</creationdate><title>TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia</title><author>Guo, Ai ; Huang, Ke ; Lu, Quanyi ; Tao, Bailong ; Li, Kai ; Jiang, Dianming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4043-d8b5b374afeeffd49511383c6a25259a95775cbf2e7a1d5a065505234aa87ccd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antibodies</topic><topic>Antioxidants</topic><topic>Biotechnology</topic><topic>Body composition</topic><topic>Cell growth</topic><topic>Homeostasis</topic><topic>Laboratory animals</topic><topic>Medical research</topic><topic>Microscopy</topic><topic>Muscle atrophy</topic><topic>Musculoskeletal system</topic><topic>Nitric oxide</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Penicillin</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Sarcopenia</topic><topic>Senescence</topic><topic>TRIM16</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Ai</creatorcontrib><creatorcontrib>Huang, Ke</creatorcontrib><creatorcontrib>Lu, Quanyi</creatorcontrib><creatorcontrib>Tao, Bailong</creatorcontrib><creatorcontrib>Li, Kai</creatorcontrib><creatorcontrib>Jiang, Dianming</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley-Blackwell Open Access Backfiles (Open Access)</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest - Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of cachexia, sarcopenia and muscle</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Ai</au><au>Huang, Ke</au><au>Lu, Quanyi</au><au>Tao, Bailong</au><au>Li, Kai</au><au>Jiang, Dianming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia</atitle><jtitle>Journal of cachexia, sarcopenia and muscle</jtitle><addtitle>J Cachexia Sarcopenia Muscle</addtitle><date>2024-10</date><risdate>2024</risdate><volume>15</volume><issue>5</issue><spage>2056</spage><epage>2070</epage><pages>2056-2070</pages><issn>2190-5991</issn><issn>2190-6009</issn><eissn>2190-6009</eissn><abstract><![CDATA[Background
Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating antioxidant responses to mitigate oxidative stress, yet its regulatory role in skeletal muscle remains unclear. This study aims to elucidate the impact of TRIM16 on enhancing antioxidant response through SIRT‐1, consequently mitigating age‐related oxidative stress, and ameliorating muscle atrophy.
Methods
Aged mouse models were established utilizing male mice at 18 months with D‐galactose (D‐gal, 200 mg/kg) intervention and at 24 months with natural aging, while 3‐month‐old young mice served as controls. Muscle cell senescence was induced in C2C12 myoblasts using 30 g/L D‐gal. TRIM16 was overexpressed in the skeletal muscle of aged mice and silenced/overexpressed in C2C12 myoblasts. The effects of TRIM16 on skeletal muscle mass, grip strength, morphological changes, myotube formation, myogenic differentiation, and muscle atrophy indicators were evaluated. Reactive oxygen species (ROS) levels and oxidative stress‐related parameters were measured. The SIRT‐1 inhibitor EX‐527 was employed to elucidate the protective role of TRIM16 mediated through SIRT‐1.
Results
Aged mice displayed significant reductions in lean mass (−11.58%; −14.47% vs. young, P < 0.05), hindlimb lean mass (−17.38%; −15.95% vs. young, P < 0.05), and grip strength (−22.29%; −31.45% vs. young, P < 0.01). Skeletal muscle fibre cross‐sectional area (CSA) decreased (−29.30%; −24.12% vs. young, P < 0.05). TRIM16 expression significantly decreased in aging skeletal muscle (−56.82%; −66.27% vs. young, P < 0.001) and senescent muscle cells (−46.53% vs. control, P < 0.001). ROS levels increased (+69.83% vs. control, P < 0.001), and myotube formation decreased in senescent muscle cells (−56.68% vs. control, P < 0.001). Expression of myogenic differentiation and antioxidant indicators decreased, while muscle atrophy markers increased in vivo and in vitro (all P < 0.05). Silencing TRIM16 in myoblasts induced oxidative stress and myotube atrophy, while TRIM16 overexpression partially mitigated aging effects on skeletal muscle. TRIM16 activation enhanced SIRT‐1 expression (+75.38% vs. control, P < 0.001). SIRT‐1 inhibitor EX‐527 (100 μM) suppressed TRIM16's antioxidant response and mitigating muscle atrophy, offsetting the protective effect of TRIM16 on senescent muscle cells.
Conclusions
This study elucidates TRIM16's role in mitigating oxidative stress and ameliorating muscle atrophy through the activation of SIRT‐1‐dependent antioxidant effects. TRIM16 emerges as a potential therapeutic target for age‐related sarcopenia.]]></abstract><cop>Germany</cop><pub>John Wiley & Sons, Inc</pub><pmid>39192479</pmid><doi>10.1002/jcsm.13553</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-9935-7066</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 2190-5991 |
| ispartof | Journal of cachexia, sarcopenia and muscle, 2024-10, Vol.15 (5), p.2056-2070 |
| issn | 2190-5991 2190-6009 2190-6009 |
| language | eng |
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| source | Wiley Online Library Open Access; ProQuest - Publicly Available Content Database; PubMed Central |
| subjects | Antibodies Antioxidants Biotechnology Body composition Cell growth Homeostasis Laboratory animals Medical research Microscopy Muscle atrophy Musculoskeletal system Nitric oxide Original Oxidative stress Penicillin Proteins Reactive oxygen species Sarcopenia Senescence TRIM16 |
| title | TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia |
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