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Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding proteins: roles in skeletal muscle growth and differentiation.
- Source :
-
General and comparative endocrinology [Gen Comp Endocrinol] 2010 Jul 01; Vol. 167 (3), pp. 344-51. Date of Electronic Publication: 2010 Apr 18. - Publication Year :
- 2010
-
Abstract
- The insulin-like growth factor (IGF) signaling pathway consists of multiple IGF ligands, IGF receptors, and IGF-binding proteins (IGFBPs). Studies in a variety of animal and cellular systems suggest that the IGF signaling pathway plays a key role in regulating skeletal muscle growth, differentiation, and in maintaining homeostasis of the adult muscle tissues. Intriguingly, IGFs stimulate both myoblast proliferation and differentiation, which are two mutually exclusive biological events during myogenesis. Both of these actions are mediated through the same IGF-1 receptor. Recent studies have shed new insights into the molecular mechanisms underlying these paradoxical actions of IGFs in muscle cells. In this article, we provide a brief review of our current understanding of the IGF signaling system and discuss recent findings on how local oxygen availability and IGFBPs act to specify IGF actions in muscle cells.<br /> ((c) 2010 Elsevier Inc. All rights reserved.)
- Subjects :
- Animals
Insulin-Like Growth Factor Binding Proteins genetics
Insulin-Like Growth Factor Binding Proteins metabolism
Models, Biological
Muscle, Skeletal metabolism
Muscle, Skeletal physiology
Receptors, Somatomedin genetics
Receptors, Somatomedin metabolism
Signal Transduction genetics
Signal Transduction physiology
Somatomedins genetics
Somatomedins metabolism
Cell Differentiation genetics
Insulin-Like Growth Factor Binding Proteins physiology
Muscle, Skeletal growth & development
Receptors, Somatomedin physiology
Somatomedins physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1095-6840
- Volume :
- 167
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- General and comparative endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 20403355
- Full Text :
- https://doi.org/10.1016/j.ygcen.2010.04.009