{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T03:21:03Z","timestamp":1791429663511,"version":"4.3.3"},"reference-count":36,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2025,5,30]],"date-time":"2025-05-30T00:00:00Z","timestamp":1748563200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["AG062413"],"award-info":[{"award-number":["AG062413"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["AG076515"],"award-info":[{"award-number":["AG076515"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["AG086085"],"award-info":[{"award-number":["AG086085"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK128552"],"award-info":[{"award-number":["DK128552"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Although animal studies have linked cellular senescence to the pathogenesis and complications of type 2 diabetes mellitus (T2DM), there is a paucity of corroborating data in humans. Thus, we measured a previously validated marker for senescent cell burden in humans, T\u2010cell expression of\n                    <jats:italic>p16<\/jats:italic>\n                    mRNA, along with additional biomarkers, to compare the senescence phenotypes of postmenopausal control (lean,\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200937) and T2DM (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200927) participants. To control for effects of obesity alone, we included a third group of obese but non\u2010diabetic women (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200929) who were matched for body mass index to the T2DM participants. In addition, given the increase in fracture risk in T2DM despite preserved or even increased bone mineral density, we related these senescence biomarkers in the T2DM participants to skeletal microarchitectural parameters. Relative to the lean participants, T\u2010cell\n                    <jats:italic>p16<\/jats:italic>\n                    and\n                    <jats:italic>p21<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Cip1<\/jats:italic>\n                    <\/jats:sup>\n                    expression was increased in the T2DM, but not the obese, non\u2010diabetic participants. Expression of\n                    <jats:italic>p16<\/jats:italic>\n                    and\n                    <jats:italic>p21<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Cip1<\/jats:italic>\n                    <\/jats:sup>\n                    was positively associated with HbA1c and an index of skin advanced glycation end\u2010products. T2DM was also associated with an increase in a number of SASP factors. Among participants with T2DM, women in the highest tertile for T\u2010cell expression of\n                    <jats:italic>p16<\/jats:italic>\n                    had significantly reduced tibial cortical area and thickness as compared to those in the lower two tertiles. Overall, our studies link cellular senescence to metabolic and skeletal alterations in T2DM and point to the need for further studies evaluating the role of cellular senescence in mediating skeletal fragility, as well as potentially other complications in T2DM.\n                  <\/jats:p>","DOI":"10.1111\/acel.70120","type":"journal-article","created":{"date-parts":[[2025,5,31]],"date-time":"2025-05-31T00:48:43Z","timestamp":1748652523000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Biomarkers of Cellular Senescence in Type 2 Diabetes Mellitus"],"prefix":"10.1111","volume":"24","author":[{"given":"Caroline","family":"Hoong","sequence":"first","affiliation":[{"name":"Division of Endocrinology Mayo Clinic  Rochester Minnesota USA"},{"name":"Robert and Arlene Kogod Center on Aging Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua N.","family":"Farr","sequence":"additional","affiliation":[{"name":"Division of Endocrinology Mayo Clinic  Rochester Minnesota USA"},{"name":"Robert and Arlene Kogod Center on Aging Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David G.","family":"Monroe","sequence":"additional","affiliation":[{"name":"Division of Endocrinology Mayo Clinic  Rochester Minnesota USA"},{"name":"Robert and Arlene Kogod Center on Aging Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A.","family":"White","sequence":"additional","affiliation":[{"name":"Robert and Arlene Kogod Center on Aging Mayo Clinic  Rochester Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth J.","family":"Atkinson","sequence":"additional","affiliation":[{"name":"Department of Quantitative Health Sciences Mayo Clinic  Rochester Minnesota 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