BMB Rep. 2015; 48(3): 131-138  
Role of histone deacetylase 2 and its posttranslational modifications in cardiac hypertrophy
Gwang Hyeon Eom* & Hyun Kook*
Department of Pharmacology and Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea
Correspondence to: Hyun Kook, Tel: +82-62-220-4242; Fax: +82-62-232-6974; E-mail:, Gwang Hyeon Eom, Tel: +82-62-220-4237, Fax: +82-62-232-6974, E-mail:
Received: November 10, 2014; Published online: March 31, 2015.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Cardiac hypertrophy is a form of global remodeling, although the initial step seems to be an adaptation to increased hemodynamic demands. The characteristics of cardiac hypertrophy include the functional reactivation of the arrested fetal gene program, where histone deacetylases (HDACs) are closely linked in the development of the process. To date, mammalian HDACs are divided into four classes: I, II, III, and IV. By structural similarities, class II HDACs are then subdivided into IIa and IIb. Among class I and II HDACs, HDAC2, 4, 5, and 9 have been reported to be involved in hypertrophic responses; HDAC4, 5, and 9 are negative regulators, whereas HDAC2 is a pro-hypertrophic mediator. The molecular function and regulation of class IIa HDACs depend largely on the phosphorylation-mediated cytosolic redistribution, whereas those of HDAC2 take place primarily in the nucleus. In response to stresses, posttranslational modification (PTM) processes, dynamic modifications after the translation of proteins, are involved in the regulation of the activities of those hypertrophy-related HDACs. In this article, we briefly review 1) the activation of HDAC2 in the development of cardiac hypertrophy and 2) the PTM of HDAC2 and its implications in the regulation of HDAC2 activity.
Keywords: Cardiac hypertrophy, Histone deacetylases, Histone deacetylase inhibitors, Posttranslational modifications

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