{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T13:14:59Z","timestamp":1792761299093,"version":"4.5.0"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2021,10,2]],"date-time":"2021-10-02T00:00:00Z","timestamp":1633132800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP20H03406"],"award-info":[{"award-number":["JP20H03406"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2021,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Sarcopenia with chronic kidney disease (CKD) progression is associated with life prognosis. Oxidative stress has attracted interest as a trigger for causing CKD\u2010related muscular atrophy. Advanced oxidation protein products (AOPPs), a uraemic toxin, are known to increase oxidative stress. However, the role of AOPPs on CKD\u2010induced muscle atrophy remains unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In a retrospective case\u2013control clinical study, we evaluated the relationship between serum AOPPs levels and muscle strength in haemodialysis patients with sarcopenia (<jats:italic>n<\/jats:italic>\u00a0=\u00a026, mean age\u00a0\u00b1\u00a0SEM: 78.5\u00a0\u00b1\u00a01.4\u00a0years for male patients; <jats:italic>n<\/jats:italic>\u00a0=\u00a022, mean age\u00a0\u00b1\u00a0SEM: 79.1\u00a0\u00b1\u00a01.5 for female patients), pre\u2010sarcopenia (<jats:italic>n<\/jats:italic>\u00a0=\u00a012, mean age\u00a0\u00b1\u00a0SEM: 73.8\u00a0\u00b1\u00a02.0\u00a0years for male patients; <jats:italic>n<\/jats:italic>\u00a0=\u00a04, mean age\u00a0\u00b1\u00a0SEM: 74.3\u00a0\u00b1\u00a04.1 for female patients) or without sarcopenia (<jats:italic>n<\/jats:italic>\u00a0=\u00a012, mean age\u00a0\u00b1\u00a0SEM: 71.3\u00a0\u00b1\u00a01.6\u00a0years for male patients; <jats:italic>n<\/jats:italic>\u00a0=\u00a07, mean age\u00a0\u00b1\u00a0SEM: 77.7\u00a0\u00b1\u00a01.6 for female ). The molecular mechanism responsible for the AOPPs\u2010induced muscle atrophy was investigated by using 5\/6\u2010nephrectomized CKD mice, AOPPs\u2010overloaded mice, and C2C12 mouse myoblast cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The haemodialysis patients with sarcopenia showed higher serum AOPPs levels as compared with the patients without sarcopenia. The serum AOPPs levels showed a negative correlation with grip strength (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01 for male patients, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01 for female patients) and skeletal muscle index (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01 for male patients). Serum AOPPs levels showed a positive correlation with cysteinylated albumin (Cys\u2010albumin), a marker of oxidative stress (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup>\u00a0=\u00a00.398, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01). In the gastrocnemius of CKD mice, muscle AOPPs levels were also increased, and it showed a positive correlation with atrogin\u20101 (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup>\u00a0=\u00a00.538, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01) and myostatin expression (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup>\u00a0=\u00a00.421, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), but a negative correlation with PGC\u20101\u03b1 expression (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup>\u00a0=\u00a00.405, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). Using C2C12 cells, AOPPs increased atrogin\u20101 and myostatin expression through the production of reactive oxygen species <jats:italic>via<\/jats:italic> CD36\/NADPH oxidase pathway, and decreased myotube formation. AOPPs also induced mitochondrial dysfunction. In the AOPPs\u2010overloaded mice showed that decreasing running time and hanging time accompanied by increasing AOPPs levels and decreasing cross\u2010sectional area in gastrocnemius.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Advanced oxidation protein products contribute to CKD\u2010induced sarcopenia, suggesting that AOPPs or its downstream signalling pathway could be a therapeutic target for the treatment of CKD\u2010induced sarcopenia. Serum AOPPs or Cys\u2010albumin levels could be a new diagnostic marker for sarcopenia in CKD.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12786","type":"journal-article","created":{"date-parts":[[2021,10,4]],"date-time":"2021-10-04T10:49:04Z","timestamp":1633344544000},"page":"1832-1847","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Advanced oxidation protein products contribute to chronic kidney disease\u2010induced muscle atrophy by inducing oxidative stress <i>via<\/i> CD36\/NADPH oxidase pathway"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6765-3223","authenticated-orcid":false,"given":"Hiromasa","family":"Kato","sequence":"first","affiliation":[{"name":"Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences Kumamoto University  Kumamoto 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