Journal
FEBS LETTERS
Volume 586, Issue 6, Pages 866-874Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2012.02.014
Keywords
Nmnat2; Cardiac hypertrophy; Sirtuin 6; NAD; Ang II
Funding
- National Natural Science Foundation of China [81072641]
- NSFC-CIHR CHINA-CANADA Joint Health Research Initiative Proposal [330811120434]
- Major Project of Guangdong Province [2008A030201013]
- Major Project of Guangzhou City [2008Z1-E571]
- National Science and Technology Major Project of China Key New Drug Creation and Manufacturing Program [2009ZX09102-152, 2011ZX09401-307]
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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. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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