{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T00:31:50Z","timestamp":1793233910786,"version":"4.5.0"},"reference-count":523,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2024,5,8]],"date-time":"2024-05-08T00:00:00Z","timestamp":1715126400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"The National Institutes of Health","award":["F31DK131914"],"award-info":[{"award-number":["F31DK131914"]}]},{"name":"The National Institutes of Health","award":["R01DK125459"],"award-info":[{"award-number":["R01DK125459"]}]},{"name":"The National Institutes of Health","award":["R01HL145528"],"award-info":[{"award-number":["R01HL145528"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Chronic kidney disease (CKD) is associated with significant reductions in lean body mass and in the mass of various tissues, including skeletal muscle, which causes fatigue and contributes to high mortality rates. In CKD, the cellular protein turnover is imbalanced, with protein degradation outweighing protein synthesis, leading to a loss of protein and cell mass, which impairs tissue function. As CKD itself, skeletal muscle wasting, or sarcopenia, can have various origins and causes, and both CKD and sarcopenia share common risk factors, such as diabetes, obesity, and age. While these pathologies together with reduced physical performance and malnutrition contribute to muscle loss, they cannot explain all features of CKD-associated sarcopenia. Metabolic acidosis, systemic inflammation, insulin resistance and the accumulation of uremic toxins have been identified as additional factors that occur in CKD and that can contribute to sarcopenia. Here, we discuss the elevation of systemic phosphate levels, also called hyperphosphatemia, and the imbalance in the endocrine regulators of phosphate metabolism as another CKD-associated pathology that can directly and indirectly harm skeletal muscle tissue. To identify causes, affected cell types, and the mechanisms of sarcopenia and thereby novel targets for therapeutic interventions, it is important to first characterize the precise pathologic changes on molecular, cellular, and histologic levels, and to do so in CKD patients as well as in animal models of CKD, which we describe here in detail. We also discuss the currently known pathomechanisms and therapeutic approaches of CKD-associated sarcopenia, as well as the effects of hyperphosphatemia and the novel drug targets it could provide to protect skeletal muscle in CKD.<\/jats:p>","DOI":"10.3390\/ijms25105117","type":"journal-article","created":{"date-parts":[[2024,5,8]],"date-time":"2024-05-08T12:27:11Z","timestamp":1715171231000},"page":"5117","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Skeletal Muscle Injury in Chronic Kidney Disease\u2014From Histologic Changes to Molecular Mechanisms and to Novel Therapies"],"prefix":"10.3390","volume":"25","author":[{"given":"Kylie","family":"Heitman","sequence":"first","affiliation":[{"name":"Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7406-5171","authenticated-orcid":false,"given":"Matthew S.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Division of Neurology, Department of Pediatrics, The University of Alabama at Birmingham and Children\u2019s of Alabama, Birmingham, AL 35294, USA"},{"name":"Center for Exercise Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"},{"name":"Department of Genetics, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"},{"name":"Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"},{"name":"Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7512-0977","authenticated-orcid":false,"given":"Christian","family":"Faul","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,5,8]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"473","DOI":"10.7326\/M16-0273","article-title":"Trends in Prevalence of Chronic Kidney Disease in the United States","volume":"165","author":"Murphy","year":"2016","journal-title":"Ann. 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