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Nmnat2 protects cardiomyocytes from hypertrophy via activation of SIRT6.

Authors: Cai, Yi  Yu, Shan-Shan  Chen, Shao-Rui  Pi, Rong-Biao  Gao, Si  Li, Hong  Ye, Jian-Tao  Liu, Pei-Qing 
Citation: Cai Y, etal., FEBS Lett. 2012 Mar 23;586(6):866-74. doi: 10.1016/j.febslet.2012.02.014. Epub 2012 Feb 20.
Pubmed: (View Article at PubMed) PMID:22449973
DOI: Full-text: DOI:10.1016/j.febslet.2012.02.014

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.


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CRRD Object Information
CRRD ID: 13782043
Created: 2018-08-15
Species: All species
Last Modified: 2018-08-15
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.