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Nmnat2 protects cardiomyocytes from hypertrophy via activation of SIRT6
Author(s) -
Cai Yi,
Yu Shan-Shan,
Chen Shao-Rui,
Pi Rong-Biao,
Gao Si,
Li Hong,
Ye Jian-Tao,
Liu Pei-Qing
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.02.014
Subject(s) - nad+ kinase , nicotinamide mononucleotide , nicotinamide adenine dinucleotide , intracellular , nicotinamide , enzyme , chemistry , biochemistry , angiotensin ii , microbiology and biotechnology , biology , receptor
The discovery of sirtuins (SIRT), a family of nicotinamide adenine dinucleotide (NAD)‐dependent deacetylases, has indicated that intracellular NAD level is crucial for the hypertrophic response of cardiomyocytes. Nicotinamide mononucleotide adenylyltransferase (Nmnat) is a central enzyme in NAD biosynthesis. Here we revealed that Nmnat2 protein expression and enzyme activity were down‐regulated during cardiac hypertrophy. In neonatal rat cardiomyocytes, overexpression of Nmnat2 but not its catalytically inactive mutant blocked angiotensin II (Ang II)‐induced cardiac hypertrophy, which was dependent on activation of SIRT6 through maintaining the intracellular NAD level. Our results suggested that modulation of Nmnat2 activity may be beneficial in cardiac hypertrophy.