Skip Navigation

Cardiovascular Research 2005 68(3):347-349; doi:10.1016/j.cardiores.2005.09.007
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Gaussin, V.
Right arrow Articles by Depre, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gaussin, V.
Right arrow Articles by Depre, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2005, European Society of Cardiology

Myostatin, the cardiac chalone of insulin-like growth factor-1

Vinciane Gaussin and Christophe Depre*

Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry New Jersey, New Jersey Medical School, 185 South Orange Street, MSB G-609, Newark, NJ 07103, United States

* Corresponding author. Tel.: +1 973 972 3926; fax: +1 973 972 7489. Email address: deprech@umdnj.edu

Received 4 August 2005; accepted 16 September 2005

The first 10% of the full text of this article appears below.

See article by Shyu et al. [2] (pages 405–414) in this issue.

In the 1960s, Bullough introduced the concept of chalones, inhibitors of cell growth that provide a negative feedback mechanism to control the size of a specific tissue [1]. In a very elegant study in this issue, Shu et al. [2] demonstrate that myostatin represents a chalone of the insulin-like growth factor-1 (IGF-1) pathway in the heart.

The IGF-1 signaling pathway, as summarized in Fig. 1A, represents an important physiological mechanism of cardiac cell growth that is initiated upon binding of IGF-1 to a tyrosine–kinase receptor (IGFR) very similar to the insulin receptor. When activated, the IGFR phosphorylates the insulin receptor . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Physiol.Home page
B. D. Rodgers, J. P. Interlichia, D. K. Garikipati, R. Mamidi, M. Chandra, O. L. Nelson, C. E. Murry, and L. F. Santana
Myostatin represses physiological hypertrophy of the heart and excitation\#8211;contraction coupling
J. Physiol., October 15, 2009; 587(20): 4873 - 4886.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
B. D. Rodgers and D. K. Garikipati
Clinical, Agricultural, and Evolutionary Biology of Myostatin: A Comparative Review
Endocr. Rev., August 1, 2008; 29(5): 513 - 534.
[Abstract] [Full Text] [PDF]

Home page
 J EndocrinolHome page
B.-W. Wang, H. Chang, P. Kuan, and K.-G. Shyu
Angiotensin II activates myostatin expression in cultured rat neonatal cardiomyocytes via p38 MAP kinase and myocyte enhance factor 2 pathway
J. Endocrinol., April 1, 2008; 197(1): 85 - 93.
[Abstract] [Full Text] [PDF]