{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T21:52:36Z","timestamp":1790200356586,"version":"4.1.0"},"reference-count":60,"publisher":"Portland Press Ltd.","issue":"15","license":[{"start":{"date-parts":[[2019,7,25]],"date-time":"2019-07-25T00:00:00Z","timestamp":1564012800000},"content-version":"vor","delay-in-days":750,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,8,1]]},"abstract":"<jats:p>Inhibition of total histone deacetylases (HDACs) was phenomenally associated with the prevention of diabetic cardiomyopathy (DCM). However, which specific HDAC plays the key role in DCM remains unclear. The present study was designed to determine whether DCM can be prevented by specific inhibition of HDAC3 and to elucidate the mechanisms by which inhibition of HDAC3 prevents DCM. Type 1 diabetes OVE26 and age-matched wild-type (WT) mice were given the selective HDAC3 inhibitor RGFP966 or vehicle for 3 months. These mice were then killed immediately or 3 months later for cardiac function and pathological examination. HDAC3 activity was significantly increased in the heart of diabetic mice. Administration of RGFP966 significantly prevented DCM, as evidenced by improved diabetes-induced cardiac dysfunction, hypertrophy, and fibrosis, along with diminished cardiac oxidative stress, inflammation, and insulin resistance, not only in the mice killed immediately or 3 months later following the 3-month treatment. Furthermore, phosphorylated extracellular signal-regulated kinases (ERK) 1\/2, a well-known initiator of cardiac hypertrophy, was significantly increased, while dual specificity phosphatase 5 (DUSP5), an ERK1\/2 nuclear phosphatase, was substantially decreased in diabetic hearts. Both of these changes were prevented by RGFP966. Chromatin immunoprecipitation (ChIP) assay showed that HDAC3 inhibition elevated histone H3 acetylation on the DUSP5 gene promoter at both two time points. These findings suggest that diabetes-activated HDAC3 inhibits DUSP5 expression through deacetylating histone H3 on the primer region of DUSP5 gene, leading to the derepression of ERK1\/2 and the initiation of DCM. The present study indicates the potential application of HDAC3 inhibitor for the prevention of DCM.<\/jats:p>","DOI":"10.1042\/cs20170064","type":"journal-article","created":{"date-parts":[[2017,5,23]],"date-time":"2017-05-23T00:10:35Z","timestamp":1495498235000},"page":"1841-1857","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":123,"title":["Inhibition of HDAC3 prevents diabetic cardiomyopathy in OVE26 mice via epigenetic regulation of DUSP5-ERK1\/2 pathway"],"prefix":"10.1042","volume":"131","author":[{"given":"Zheng","family":"Xu","sequence":"first","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"},{"name":"Pediatric Research Institute at the Department of Pediatrics, the University of Louisville, Louisville, KY 40202, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Tong","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiguo","family":"Zhang","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shudong","family":"Wang","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Zheng","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiuju","family":"Liu","sequence":"additional","affiliation":[{"name":"Cancer Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling-bo","family":"Qian","sequence":"additional","affiliation":[{"name":"Pediatric Research Institute at the Department of Pediatrics, the University of Louisville, Louisville, KY 40202, U.S.A."},{"name":"Department of Basic Medical Sciences, Hangzhou Medical College, Hangzhou 310053, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shao-yu","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Alcohol Research Center, University of Louisville, Louisville, KY 40202, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Sun","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Cai","sequence":"additional","affiliation":[{"name":"Cardiovascular Center, the First Hospital of Jilin University, Changchun 130021, China"},{"name":"Pediatric Research Institute at the Department of Pediatrics, the University of Louisville, Louisville, KY 40202, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2017,7,5]]},"reference":[{"key":"2021113011050746600_B1","volume-title":"IDF Diabetes ATLAS","author":"International Diabetes Federation","year":"2015","edition":"7th edn"},{"key":"2021113011050746600_B2","doi-asserted-by":"crossref","first-page":"13a","DOI":"10.1016\/j.amjcard.2003.11.003","article-title":"Diabetic cardiomyopathy: a metabolic perspective","volume":"93","author":"Avogaro","year":"2004","journal-title":"Am. 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