{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T22:12:11Z","timestamp":1780438331942,"version":"3.54.1"},"reference-count":38,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,4,19]],"date-time":"2023-04-19T00:00:00Z","timestamp":1681862400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Kaohsiung J of Med Scie"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Diabetic cardiomyopathy (DCM) is a serious cardiovascular complication of diabetes that severely affects the quality of life of diabetic patients. Long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of DCM. However, the role of the lncRNA homeobox transcript antisense RNA (HOTAIR) in the progression of DCM remains unclear. The present study aimed to investigate the role of HOTAIR in high glucose (HG)\u2010induced pyroptosis in cardiomyocytes. The expression of the lncRNA HOTAIR, FUS, and SIRT3 in H9C2 cardiomyocytes was detected by RT\u2013qPCR. Western blotting was used to evaluate the expression of FUS and SIRT3 as well as that of pyroptosis\u2010 and inflammation\u2010related proteins. RT\u2013qPCR and ELISA were used to determine the expression and secretion of IL\u20101\u03b2 and IL\u201018. RNA pulldown and RIP experiments were used to validate the binding relationship among HOTAIR, FUS, and SIRT3. Flow cytometry was performed to detect pyroptosis. HG induced pyroptosis and elevated the expression of proteins associated with pyroptosis and inflammation (NLRP3, GSDMD\u2010N, cleaved caspase\u20101, IL\u20101\u03b2, and IL\u201018) in cardiomyocytes. HOTAIR and SIRT3 levels were decreased in HG\u2010exposed H9C2 cells. Additionally, overexpression of HOTAIR inhibited the HG\u2010induced pyroptosis and inflammatory response in cardiomyocytes. HOTAIR upregulated SIRT3 expression in H9C2 cells by targeting FUS. Moreover, SIRT3 upregulation suppressed HG\u2010mediated pyroptosis of cardiomyocytes. Notably, SIRT3 depletion reversed the inhibitory effect of HOTAIR on HG\u2010triggered pyroptosis in cardiomyocytes. Our research indicates that HOTAIR alleviates pyroptosis in diabetic cardiomyocytes through the FUS\/SIRT3 axis, providing a potential marker for the diagnosis and treatment of DCM.<\/jats:p>","DOI":"10.1002\/kjm2.12676","type":"journal-article","created":{"date-parts":[[2023,4,19]],"date-time":"2023-04-19T10:00:55Z","timestamp":1681898455000},"page":"458-467","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["The lncRNA HOTAIR attenuates pyroptosis of diabetic cardiomyocytes by recruiting FUS to regulate SIRT3 expression"],"prefix":"10.1002","volume":"39","author":[{"given":"Jing","family":"Xiong","sequence":"first","affiliation":[{"name":"Department of Endocrinology Third Xiangya Hospital  Changsha Hunan Province People's Republic of 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