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Histone deacetylases (HDACs) are post\u2010translational modifying enzymes that can deacetylate histones and non\u2010histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro\u2010hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Kr\u00fcppel like factor 4 (KLF4) or inositol polyphosphate\u20105\u2010phosphatase f (Inpp5f). Thus, modulators of HDAC2 enzymes, such as selective HDAC inhibitors, are considered to be an important target for heart diseases, especially for preventing cardiac hypertrophy. In contrast, class IIa HDACs have been shown to repress cardiac hypertrophy by inhibiting cardiac\u2010specific transcription factors such as myocyte enhancer factor 2 (MEF2), GATA4, and NFAT in the heart. Studies of class IIa HDACs have shown that the underlying mechanism is regulated by nucleo\u2010cytoplasm shuttling in response to a variety of stress signals. In this review, we focus on the class I and IIa HDACs that play critical roles in mediating cardiac hypertrophy and discuss the non\u2010histone targets of HDACs in heart disease.<\/jats:p>","DOI":"10.1155\/2011\/928326","type":"journal-article","created":{"date-parts":[[2010,11,29]],"date-time":"2010-11-29T14:36:35Z","timestamp":1291041395000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy"],"prefix":"10.1155","volume":"2011","author":[{"given":"Hae 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