{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T09:05:08Z","timestamp":1791363908944,"version":"4.3.1"},"reference-count":61,"publisher":"American Society for Cell Biology (ASCB)","issue":"24","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MBoC"],"published-print":{"date-parts":[[2013,12,15]]},"abstract":"<jats:p> The development and progression of cardiac hypertrophy often leads to heart failure and death, and important modulators of hypertrophy include the histone deacetylase proteins (HDACs). Estrogen inhibits cardiac hypertrophy and progression in animal models and humans. We therefore investigated the influence of 17-\u03b2-estradiol on the production, localization, and functions of prohypertrophic (class I) and antihypertrophic (class II) HDACs in cultured neonatal rat cardiomyocytes. 17-\u03b2-Estradiol or estrogen receptor \u03b2 agonists dipropylnitrile and \u03b2-LGND2 comparably suppressed angiotensin II\u2013induced HDAC2 (class I) production, HDAC-activating phosphorylation, and the resulting prohypertrophic mRNA expression. In contrast, estrogenic compounds derepressed the opposite effects of angiotensin II on the same parameters for HDAC4 and 5 (class II), resulting in retention of these deacetylases in the nucleus to inhibit hypertrophic gene expression. Key aspects were confirmed in vivo from the hearts of wild-type but not estrogen receptor \u03b2 (ER\u03b2) gene\u2013deleted mice administered angiotensin II and estrogenic compounds. Our results identify a novel dual regulation of cardiomyocyte HDACs, shown here for the antihypertrophic sex steroid acting at ER\u03b2. This mechanism potentially supports using ER\u03b2 agonists as HDAC modulators to treat cardiac disease. <\/jats:p>","DOI":"10.1091\/mbc.e13-08-0444","type":"journal-article","created":{"date-parts":[[2013,10,24]],"date-time":"2013-10-24T02:57:00Z","timestamp":1382583420000},"page":"3805-3818","source":"Crossref","is-referenced-by-count":75,"title":["Estrogen regulates histone deacetylases to prevent cardiac hypertrophy"],"prefix":"10.1091","volume":"24","author":[{"given":"Ali","family":"Pedram","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, University of California, Irvine, Irvine, CA 92717"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahnaz","family":"Razandi","sequence":"additional","affiliation":[{"name":"Department of Veterans Affairs Medical Center, Long Beach, CA 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