{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T15:04:09Z","timestamp":1783523049636,"version":"3.55.0"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2015,11,19]],"date-time":"2015-11-19T00:00:00Z","timestamp":1447891200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2016,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Muscle wasting during cancer cachexia contributes to patient morbidity. Cachexia\u2010induced muscle damage may be understood by comparing its symptoms with those of other skeletal muscle diseases, but currently available data are limited.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We modelled cancer cachexia in mice bearing Lewis lung carcinoma\/colon adenocarcinoma and compared the associated muscle damage with that in a murine muscular dystrophy model (<jats:italic>mdx<\/jats:italic> mice). We measured biochemical and immunochemical parameters: amounts\/localization of cytoskeletal proteins and\/or Ca<jats:sup>2+<\/jats:sup> signalling proteins related to muscle function and abnormality. We analysed intracellular Ca<jats:sup>2+<\/jats:sup> mobilization and compared results between the two models. Involvement of Ca<jats:sup>2+<\/jats:sup>\u2010permeable channel transient receptor potential vanilloid 2 (TRPV2) was examined by inoculating Lewis lung carcinoma cells into transgenic mice expressing dominant\u2010negative TRPV2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Tumourigenesis caused loss of body and skeletal muscle weight and reduced muscle force and locomotor activity. Similar to <jats:italic>mdx<\/jats:italic> mice, cachexia muscles exhibited myolysis, reduced sarcolemmal sialic acid content, and enhanced lysosomal exocytosis and sarcolemmal localization of phosphorylated Ca<jats:sup>2+<\/jats:sup>\/CaMKII. Abnormal autophagy and degradation of dystrophin also occurred. Unlike <jats:italic>mdx<\/jats:italic> muscles, cachexia muscles did not exhibit regeneration markers (centrally nucleated fibres), and levels of autophagic proteolytic pathway markers increased. While a slight accumulation of TRPV2 was observed in cachexia muscles, Ca<jats:sup>2+<\/jats:sup> influx via TRPV2 was not elevated in cachexia\u2010associated myotubes, and the course of cachexia pathology was not ameliorated by dominant\u2010negative inhibition of TRPV2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Thus, cancer cachexia may induce muscle damage through TRPV2\u2010independent mechanisms distinct from those in muscular dystrophy; this may help treat patients with tumour\u2010induced muscle wasting.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12067","type":"journal-article","created":{"date-parts":[[2015,11,19]],"date-time":"2015-11-19T05:22:47Z","timestamp":1447910567000},"page":"366-376","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Cancer cachexia causes skeletal muscle damage via transient receptor potential vanilloid 2\u2010independent mechanisms, unlike muscular dystrophy"],"prefix":"10.1002","volume":"7","author":[{"given":"Yuko","family":"Iwata","sequence":"first","affiliation":[{"name":"Department of Molecular Physiology National Cerebral and Cardiovascular Center Research Institute Suita  Osaka 565\u20108565 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuyuki","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Kyowa Hakko Kirin CO. Ltd  Chiyoda\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hitomi","family":"Ohtake","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology National Cerebral and Cardiovascular Center Research Institute Suita  Osaka 565\u20108565 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinya","family":"Kamauchi","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology National Cerebral and Cardiovascular Center Research Institute Suita  Osaka 565\u20108565 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naohiro","family":"Hashimoto","sequence":"additional","affiliation":[{"name":"Department of Regenerative Medicine, National Institute for Longevity Science National Center for Geriatrics and Gerontology  Oobu Aichi 474\u20108522 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