Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation
Chronic inflammation is a hallmark of cancer cachexia in both patients and preclinical models. Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulat...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2017-01, Vol.2017 (2017), p.1-13 |
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| creator | VanderVeen, Brandon N. Carson, James A. Fix, Dennis K. |
| description | Chronic inflammation is a hallmark of cancer cachexia in both patients and preclinical models. Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulation of cancer cachexia. An established characteristic of cachectic skeletal muscle is a disrupted capacity for oxidative metabolism, which is thought to contribute to cancer patient fatigue, diminished metabolic function, and muscle mass loss. This review’s primary objective is to highlight emerging evidence linking cancer-induced inflammation to the dysfunctional regulation of mitochondrial dynamics, mitophagy, and biogenesis in cachectic muscle. The potential for either muscle inactivity or exercise to alter mitochondrial dysfunction during cancer cachexia will also be discussed. |
| doi_str_mv | 10.1155/2017/3292087 |
| format | Article |
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Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulation of cancer cachexia. An established characteristic of cachectic skeletal muscle is a disrupted capacity for oxidative metabolism, which is thought to contribute to cancer patient fatigue, diminished metabolic function, and muscle mass loss. This review’s primary objective is to highlight emerging evidence linking cancer-induced inflammation to the dysfunctional regulation of mitochondrial dynamics, mitophagy, and biogenesis in cachectic muscle. The potential for either muscle inactivity or exercise to alter mitochondrial dysfunction during cancer cachexia will also be discussed.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2017/3292087</identifier><identifier>PMID: 28785374</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Autophagy ; Biosynthesis ; Cachexia ; Cachexia - pathology ; Cancer ; Care and treatment ; Chronic illnesses ; Cytokines ; Development and progression ; Disease ; Exercise ; Gangrene ; Genetic aspects ; Health aspects ; Homeostasis ; Humans ; Immunity ; Inflammation ; Inflammation - pathology ; Investigations ; Metabolism ; Mitochondria ; Mitochondrial Degradation ; Mitochondrial Dynamics ; Muscle contraction ; Musculoskeletal system ; Neoplasms - pathology ; Organelle Biogenesis ; Physical fitness ; Review ; Rodents ; Tumor necrosis factor-TNF</subject><ispartof>Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-13</ispartof><rights>Copyright © 2017 Brandon N. VanderVeen et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Brandon N. VanderVeen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Brandon N. VanderVeen et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-4fe554f6ba9c534808fb6b2b89399035bbc01e5e3fb3667236fdf118d4458883</citedby><cites>FETCH-LOGICAL-c565t-4fe554f6ba9c534808fb6b2b89399035bbc01e5e3fb3667236fdf118d4458883</cites><orcidid>0000-0003-3733-8796</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5530417/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5530417/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28785374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Malek, Moh H.</contributor><creatorcontrib>VanderVeen, Brandon N.</creatorcontrib><creatorcontrib>Carson, James A.</creatorcontrib><creatorcontrib>Fix, Dennis K.</creatorcontrib><title>Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Chronic inflammation is a hallmark of cancer cachexia in both patients and preclinical models. Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulation of cancer cachexia. An established characteristic of cachectic skeletal muscle is a disrupted capacity for oxidative metabolism, which is thought to contribute to cancer patient fatigue, diminished metabolic function, and muscle mass loss. This review’s primary objective is to highlight emerging evidence linking cancer-induced inflammation to the dysfunctional regulation of mitochondrial dynamics, mitophagy, and biogenesis in cachectic muscle. The potential for either muscle inactivity or exercise to alter mitochondrial dysfunction during cancer cachexia will also be discussed.</description><subject>Autophagy</subject><subject>Biosynthesis</subject><subject>Cachexia</subject><subject>Cachexia - pathology</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Chronic illnesses</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Exercise</subject><subject>Gangrene</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Immunity</subject><subject>Inflammation</subject><subject>Inflammation - pathology</subject><subject>Investigations</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondrial Degradation</subject><subject>Mitochondrial Dynamics</subject><subject>Muscle contraction</subject><subject>Musculoskeletal system</subject><subject>Neoplasms - pathology</subject><subject>Organelle Biogenesis</subject><subject>Physical fitness</subject><subject>Review</subject><subject>Rodents</subject><subject>Tumor necrosis factor-TNF</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkkuP0zAURiMEYh6wY40isUGalvEzsVkglQ6PkWaEBLO3HOc69ZDYxU6Aij-PS0sHWLG61vXRsa8_F8UTjF5gzPk5Qbg-p0QSJOp7xTGWjMyRlOz-YY3QUXGS0i1CFSUMPyyOiKgFpzU7Ln5cuBSn9Qht-ekz9DDqvryekumhvHZjMKvg2-hy82Lj9eBMmv3qr1e628xK7dvytQsdeEgule0Une_KpfYGYi5mBd-dflkuyo8hC22I5aW3vR4GPbrgHxUPrO4TPN7X0-Lm7Zub5fv51Yd3l8vF1dzwio9zZoFzZqtGS8MpE0jYpmpIIySVElHeNAZh4EBtQ6uqJrSyrcVYtIxxIQQ9LV7ttOupGaA14Meoe7WObtBxo4J26u8d71aqC18V5xQxXGfB870ghi8TpFENLhnoe-0hTElhSWqK8ouSjD77B70NU_R5ui1FMlLT-o7qdA_KeRvyuWYrVQvOueCISZmp2Y4yMaQUwR6ujJHaRq-20at99Bl_-ueYB_h31hk42wEr51v9zf2nDjIDVt_R-VdRJOhPynq_kg</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>VanderVeen, Brandon N.</creator><creator>Carson, James A.</creator><creator>Fix, Dennis K.</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3733-8796</orcidid></search><sort><creationdate>20170101</creationdate><title>Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation</title><author>VanderVeen, Brandon N. ; 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| subjects | Autophagy Biosynthesis Cachexia Cachexia - pathology Cancer Care and treatment Chronic illnesses Cytokines Development and progression Disease Exercise Gangrene Genetic aspects Health aspects Homeostasis Humans Immunity Inflammation Inflammation - pathology Investigations Metabolism Mitochondria Mitochondrial Degradation Mitochondrial Dynamics Muscle contraction Musculoskeletal system Neoplasms - pathology Organelle Biogenesis Physical fitness Review Rodents Tumor necrosis factor-TNF |
| title | Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation |
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