{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T07:58:12Z","timestamp":1790582292880,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T00:00:00Z","timestamp":1789344000000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82271601"],"award-info":[{"award-number":["82271601"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Diabetes accelerates cardiac aging, but the molecular mechanisms that link metabolic stress to myocardial senescence remain insufficiently defined. This study investigated factors driving diabetes\u2010associated cardiac aging with a focus on the role of USP18. Type 2 diabetes mellitus (T2DM) was induced in mice using a high\u2010fat diet combined with streptozotocin. Cardiac structure, function, and molecular alterations were evaluated by echocardiography, histology, RNA sequencing, western blotting, qPCR, and immunofluorescence. H9C2 cardiomyocytes cultured under high\u2010glucose conditions were used for in vitro validation. Diabetic mice exhibited diastolic dysfunction, myocardial hypertrophy, and fibrosis, accompanied by increased p53 and p21 expression. RNA\u2010seq and protein analyses consistently identified USP18 as significantly upregulated in diabetic hearts. Elevated USP18 was associated with activation of the cGAS\u2013STING pathway, increased TBK1 phosphorylation, and enhanced IL\u20106 and IL\u20101\u03b2 production. High\u2010glucose\u2013treated cardiomyocytes similarly showed USP18 induction, stabilization of cGAS\u2013STING signaling, and enhanced senescence\u2010related responses. USP18 contributes to cardiac aging in diabetes by promoting cGAS\u2013STING activation and inflammatory senescence. Targeting USP18 may represent a potential strategy to alleviate myocardial aging under diabetic conditions.<\/jats:p>","DOI":"10.1002\/cbf.70282","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T15:35:10Z","timestamp":1789400110000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["USP18 Serves as a Key Mediator of cGAS\u2010STING for Cardiac Aging in Diabetes"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-3766-2042","authenticated-orcid":false,"given":"Xunxi","family":"Deng","sequence":"first","affiliation":[{"name":"Department of Blood Transfusion The Second Xiangya Hospital of Central South University Changsha China"},{"name":"Department of Cardiology The Second Xiangya Hospital of Central South University Changsha 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