{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T14:53:57Z","timestamp":1787237637025,"version":"build-2736575974"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T00:00:00Z","timestamp":1777507200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100007155","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/T008172\/1"],"award-info":[{"award-number":["MR\/T008172\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000288","name":"Royal Society","doi-asserted-by":"publisher","award":["RGF\\R1\\180008"],"award-info":[{"award-number":["RGF\\R1\\180008"]}],"id":[{"id":"10.13039\/501100000288","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Royal Society Dorothy Hodgkin Fellowship","award":["DH16044"],"award-info":[{"award-number":["DH16044"]}]},{"name":"Birmingham Fellowship"},{"DOI":"10.13039\/501100000691","name":"Academy of Medical Sciences Springboard Award","doi-asserted-by":"publisher","award":["SBF003\\1156"],"award-info":[{"award-number":["SBF003\\1156"]}],"id":[{"id":"10.13039\/501100000691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000691","name":"Academy of Medical Sciences Springboard Award","doi-asserted-by":"publisher","award":["MR\/T028025\/1"],"award-info":[{"award-number":["MR\/T028025\/1"]}],"id":[{"id":"10.13039\/501100000691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000272","name":"National Institute for Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100018952","name":"Birmingham Biomedical Research Centre","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100018952","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,4,30]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Chronic kidney disease (CKD) is associated with increased incidence of sarcopenia and muscle weakness in aging patients. The glucocorticoid-activating enzyme11\u03b2-hydroxysteroid dehydrogenase type 1 (11\u03b2-HSD1) within skeletal muscle in these patients has been implicated in driving this process. We hypothesized that skeletal muscle 11\u03b2-HSD1 is elevated in CKD and aging, where it would represent a promising therapeutic target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We measured 11\u03b2-HSD1 activity in quadriceps biopsies from 17 CKD patients (eGFR &amp;lt;30\u2005mL\/min) and 14 age-matched controls (mean age 71 \u00b1 5 years). Muscle strength, mass, and gait speed were assessed in relation to tissue 11\u03b2-HSD1 activity. Primary human myotubes were treated with patient-derived sera to evaluate regulatory drivers. Murine models of CKD (adenine diet) and aging (21 months) in wild-type (WT) and 11\u03b2-HSD1 knockout (11\u03b2KO) animals were examined to model therapeutic targeting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Muscle 11\u03b2-HSD1 activity was not elevated with CKD, but increased with age (r = 0.559, P = .001), predicting lower grip strength (P = .008). Markers of inflammation, including C-reactive protein and IL-6, strongly predicted 11\u03b2-HSD1 activity. Pro-inflammatory mediators such as TNF\u03b1 directly upregulated 11\u03b2-HSD1 activity in myotubes, whilst sera from CKD donors did not. Whilst mice with 11\u03b2KO deletion were not protected from CKD-driven muscle atrophy, 11\u03b2KO animals showed marked protection against age-related muscle loss.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Skeletal muscle 11\u03b2-HSD1 activity is not induced by CKD itself, but increases significantly over aging, where it is a predictor of muscle weakness. Its targeted deletion preserves muscle mass in aged mice, supporting its efficacy in preventing sarcopenia in an aging CKD population.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ejendo\/lvag075","type":"journal-article","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T19:24:52Z","timestamp":1777577092000},"page":"627-640","source":"Crossref","is-referenced-by-count":1,"title":["Divergent roles of skeletal muscle 11\u03b2-HSD1 in age-related and chronic kidney disease-associated sarcopenia"],"prefix":"10.1093","volume":"194","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6166-6784","authenticated-orcid":false,"given":"Michael S","family":"Sagmeister","sequence":"first","affiliation":[{"name":"Department of Applied Health Sciences, School of Health Sciences, College of Medicine and Health, University of Birmingham, Birmingham , B152TT ,","place":["UK"]},{"name":"Department of Metabolism and Systems Science, School of Medical Sciences, College of Medicine 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