Please use this identifier to cite or link to this item: https://doi.org/10.1161/01.RES.0000231290.45676.d4
Title: Myostatin regulates cardiomyocyte growth through modulation of Akt signaling
Authors: Morissette M.R.
Cook S.A. 
Foo S.
McKoy G.
Ashida N.
Novikov M.
Scherrer-Crosbie M.
Li L.
Matsui T.
Brooks G.
Rosenzweig A.
Keywords: Akt
Hypertrophy
Myostatin
p38
Issue Date: 2006
Publisher: American Heart Association
Citation: Morissette M.R., Cook S.A., Foo S., McKoy G., Ashida N., Novikov M., Scherrer-Crosbie M., Li L., Matsui T., Brooks G., Rosenzweig A. (2006). Myostatin regulates cardiomyocyte growth through modulation of Akt signaling. Circulation Research 99 (1) : 15-24. ScholarBank@NUS Repository. https://doi.org/10.1161/01.RES.0000231290.45676.d4
Abstract: Myostatin is a highly conserved, potent negative regulator of skeletal muscle hypertrophy in many species, from rodents to humans, although its mechanisms of action are incompletely understood. Transcript profiling of hearts from a genetic model of cardiac hypertrophy revealed dramatic upregulation of myostatin, not previously recognized to play a role in the heart. Here we show that myostatin abrogates the cardiomyocyte growth response to phenylephrine in vitro through inhibition of p38 and the serine-threonine kinase Akt, a critical determinant of cell size in many species from drosophila to mammals. Evaluation of male myostatin-null mice revealed that their cardiomyocytes and hearts overall were slightly smaller at baseline than littermate controls but exhibited more exuberant growth in response to chronic phenylephrine infusion. The increased cardiac growth in myostatin-null mice corresponded with increased p38 phosphorylation and Akt activation in vivo after phenylephrine treatment. Together, these data demonstrate that myostatin is dynamically regulated in the heart and acts more broadly than previously appreciated to regulate growth of multiple types of striated muscle. � 2006 American Heart Association, Inc.
Source Title: Circulation Research
URI: http://scholarbank.nus.edu.sg/handle/10635/149997
ISSN: 00097330
DOI: 10.1161/01.RES.0000231290.45676.d4
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