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The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy.

Authors: Buitrago, M  Lorenz, K  Maass, AH  Oberdorf-Maass, S  Keller, U  Schmitteckert, EM  Ivashchenko, Y  Lohse, MJ  Engelhardt, S 
Citation: Buitrago M, etal., Nat Med. 2005 Aug;11(8):837-44. Epub 2005 Jul 17.
Pubmed: (View Article at PubMed) PMID:16025126
DOI: Full-text: DOI:10.1038/nm1272

Hypertrophy represents the major physiological response of the heart to adapt to chronically enhanced workload, but is also crucial in the development of heart failure. Although we know of numerous inducers of cardiac hypertrophy, little is known about mechanisms that limit cardiac hypertrophy. Here, we describe the transcriptional repressor NAB1 as an endogenous regulator of cardiac growth. We identified NAB1 as being upregulated in both mouse and human heart failure. Nab1 is highly expressed in mammalian cardiac myocytes and it inhibited cardiomyocyte hypertrophy through repression of its targets, transcription factor Egr. Transgenic mice with cardiac-specific overexpression of Nab1 showed that Nab1 is a potent inhibitor of cardiac growth in response to pathological stimuli in vivo. Nab1 overexpression suppressed adrenergically induced and pressure overload-induced hypertrophy, whereas physiological growth during development and in response to exercise was not affected. These findings implicate the Nab1-Egr1 axis as a crucial regulator of pathological cardiac growth.


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CRRD Object Information
CRRD ID: 5131654
Created: 2011-05-10
Species: All species
Last Modified: 2011-05-10
Status: ACTIVE


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