{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T04:11:19Z","timestamp":1792642279365,"version":"4.5.0"},"reference-count":50,"publisher":"Korean Endocrine Society","issue":"3","license":[{"start":{"date-parts":[[2023,6,14]],"date-time":"2023-06-14T00:00:00Z","timestamp":1686700800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK128552"],"award-info":[{"award-number":["R01 DK128552"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P01 AG062413"],"award-info":[{"award-number":["P01 AG062413"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21 AG065868"],"award-info":[{"award-number":["R21 AG065868"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["e-enm.org"],"crossmark-restriction":true},"short-container-title":["Endocrinol Metab"],"published-print":{"date-parts":[[2023,6,30]]},"abstract":"<jats:p>Osteoporosis and type 2 diabetes (T2D) are common diseases that often coexist. While both of these diseases are associated with poor bone quality and increased fracture risk, their pathogenesis of increased fracture risk differs and is multifactorial. Mounting evidence now indicates that key fundamental mechanisms that are central to both aging and energy metabolism exist. Importantly, these mechanisms represent potentially modifiable therapeutic targets for interventions that could prevent or alleviate multiple complications of osteoporosis and T2D, including poor bone quality. One such mechanism that has gained increasing momentum is senescence, which is a cell fate that contributes to multiple chronic diseases. Accumulating evidence has established that numerous boneresident cell types become susceptible to cellular senescence with old age. Recent work also demonstrates that T2D causes the premature accumulation of senescent osteocytes during young adulthood, at least in mice, although it remains to be seen which other bone-resident cell types become senescent with T2D. Given that therapeutically removing senescent cells can alleviate age-related bone loss and T2D-induced metabolic dysfunction, it will be important in future studies to rigorously test whether interventions that eliminate senescent cells can also alleviate skeletal dysfunction in context of T2D, as it does with aging.<\/jats:p>","DOI":"10.3803\/enm.2023.1727","type":"journal-article","created":{"date-parts":[[2023,6,14]],"date-time":"2023-06-14T00:11:33Z","timestamp":1686701493000},"page":"295-301","update-policy":"https:\/\/doi.org\/10.3803\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Skeletal Senescence with Aging and Type 2 Diabetes"],"prefix":"10.3803","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3179-6414","authenticated-orcid":true,"given":"Joshua Nicholas","family":"Farr","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"2119","reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.2269"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1089\/pop.2015.0181"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2015.07.027"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016\/s2213-8587(15)00283-1"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1038\/nrendo.2016.153"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1016\/j.mayocp.2022.03.011"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2013.05.039"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.3564"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1038\/s41574-020-0335-y"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2019.01.015"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1038\/s41574-021-00555-5"},{"key":"ref12","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4827(61)90192-6"},{"key":"ref13","doi-asserted-by":"publisher","DOI":"10.1172\/jci64098"},{"key":"ref14","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.24.13742"},{"key":"ref15","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg417"},{"key":"ref16","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2017.04.013"},{"key":"ref17","first-page":"2853","volume-title":"Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor","author":"Coppe","year":"2008"},{"key":"ref18","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pathol-121808-102144"},{"key":"ref19","doi-asserted-by":"publisher","DOI":"10.1038\/ncb2784"},{"key":"ref20","doi-asserted-by":"publisher","DOI":"10.1016\/j.smim.2019.04.003"},{"key":"ref21","first-page":"2284","volume-title":"Senescent human fibroblasts resist programmed cell death, and failure to suppress bcl2 is involved","author":"Wang","year":"1995"},{"key":"ref22","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.2892"},{"key":"ref23","doi-asserted-by":"publisher","DOI":"10.7554\/elife.69958"},{"key":"ref24","doi-asserted-by":"publisher","DOI":"10.1111\/acel.13602"},{"key":"ref25","doi-asserted-by":"publisher","DOI":"10.1038\/nm.4385"},{"key":"ref26","doi-asserted-by":"publisher","DOI":"10.1038\/nature10600"},{"key":"ref27","doi-asserted-by":"publisher","DOI":"10.1056\/nejmoa1002315"},{"key":"ref28","doi-asserted-by":"publisher","DOI":"10.1016\/j.fitote.2015.09.018"},{"key":"ref29","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12344"},{"key":"ref30","doi-asserted-by":"publisher","DOI":"10.7554\/elife.12997"},{"key":"ref31","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-018-0092-9"},{"key":"ref32","doi-asserted-by":"publisher","DOI":"10.1111\/acel.12950"},{"key":"ref33","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms15691"},{"key":"ref34","first-page":"129","volume-title":"Acceleration of b cell aging determines diabetes and senolysis improves disease outcomes","author":"Aguayo-Mazzucato","year":"2019"},{"key":"ref35","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2018.12.008"},{"key":"ref36","doi-asserted-by":"publisher","DOI":"10.1016\/s0026-0495(98)90027-0"},{"key":"ref37","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.135236"},{"key":"ref38","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.2106"},{"key":"ref39","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2016-1437"},{"key":"ref40","doi-asserted-by":"publisher","DOI":"10.1002\/jbmr.3057"},{"key":"ref41","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2021.11.002"},{"key":"ref42","doi-asserted-by":"publisher","DOI":"10.1016\/j.ebiom.2019.08.069"},{"key":"ref43","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-32552-1"},{"key":"ref44","doi-asserted-by":"publisher","DOI":"10.1111\/j.1474-9726.2012.00795.x"},{"key":"ref45","first-page":"30","volume-title":"The senescent bystander effect is caused by ROS-activated NF-kB signalling","author":"Nelson","year":"2018"},{"key":"ref46","doi-asserted-by":"publisher","DOI":"10.1172\/jci162519"},{"key":"ref47","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201306073"},{"key":"ref48","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms1708"},{"key":"ref49","doi-asserted-by":"publisher","DOI":"10.1517\/14728222.2016.1111873"},{"key":"ref50","doi-asserted-by":"publisher","DOI":"10.1002\/cpt.148"}],"container-title":["Endocrinology and Metabolism"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/e-enm.org\/upload\/pdf\/enm-2023-1727.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/e-enm.org\/journal\/view.php?doi=10.3803\/EnM.2023.1727","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/e-enm.org\/upload\/pdf\/enm-2023-1727.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,4]],"date-time":"2023-07-04T00:44:28Z","timestamp":1688431468000},"score":1,"resource":{"primary":{"URL":"http:\/\/e-enm.org\/journal\/view.php?doi=10.3803\/EnM.2023.1727"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2023,6,30]]},"references-count":50,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2023,6]]}},"URL":"https:\/\/doi.org\/10.3803\/enm.2023.1727","relation":{},"ISSN":["2093-596X","2093-5978"],"issn-type":[{"value":"2093-596X","type":"print"},{"value":"2093-5978","type":"electronic"}],"subject":[],"published":{"date-parts":[[2023,6,30]]},"assertion":[{"value":"2023-05-05","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-05-26","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-06-14","order":2,"name":"published","label":"Published online","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-06-30","order":3,"name":"published","label":"Print publication","group":{"name":"publication_history","label":"Publication History"}}]}}