Huetal.JZhejiangUniv-SciB.PDF

Hu et al. / J Zhejiang Univ-Sci B (Biomed Biotechnol) 2016 17(11):821-830 821 Journal of Zhejiang University-SCIENCE B (Biomedicine Biotechnology) ISSN 1673-1581 (Print); ISSN 1862-1783 (Online) /jzus; E-mail: jzus@ Review: Roles of SIRT3 in heart failure: from bench to bedside* De-xing HU?1,2,3, Xian-bao LIU1,2, Wen-chao SONG3, Jian-an WANG??1,2 (1Department of Cardiology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China) (2Provincial Key Laboratory of Cardiovascular Research of Zhejiang Province, Hangzhou 310009, China) (3Department of Cardiology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo 315100, China) ?E-mail:; jian_an_wang@ Received May 16, 2016; Revision accepted July 13, 2016; Crosschecked Oct. 18, 2016 Abstract: Heart failure (HF) represents the most common endpoint of most cardiovascular diseases (CVDs) which are the leading causes of death around the world. Despite the advances in treating CVDs, the prevalence of HF con- tinues to increase. It is believed that better results of prognosis are obtained from prevention rather than additional treatment for HF. Therefore, it is reasonable to prevent the development of CVDs or other complications to HF. Most types of HF are attributed to contractile dysfunction, cardiac hypertrophy or remodeling, and ischemic injuries. SIRT3 is a mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase whose substrates vary from met- abolic biogenesis-associated proteins to stress-responsive proteins. In recent years, a num