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J Appl Physiol 88: 337-343, 2000;
8750-7587/00 $5.00
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Vol. 88, Issue 1, 337-343, January 2000

INVITED REVIEW
Integrin signaling's potential for mediating gene expression in hypertrophying skeletal muscle

James A. Carson1 and Lei Wei2

1 Exercise Science Department, University of South Carolina, Columbia, South Carolina 29208; and 2 Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030

Overloaded skeletal muscle undergoes dramatic shifts in gene expression, which alter both the phenotype and mass. Molecular biology techniques employing both in vivo and in vitro hypertrophy models have demonstrated that mechanical forces can alter skeletal muscle gene regulation. This review's purpose is to support integrin-mediated signaling as a candidate for mechanical load-induced hypertrophy. Research quantifying components of the integrin-signaling pathway in overloaded skeletal muscle have been integrated with knowledge regarding integrins role during development and cardiac hypertrophy, with the hope of demonstrating the pathway's importance. The role of integrin signaling as an integrator of mechanical forces and growth factor signaling during hypertrophy is discussed. Specific components of integrin signaling, including focal adhesion kinase and low-molecular-weight GTPase Rho are mentioned as downstream targets of this signaling pathway. There is a need for additional mechanistic studies capable of providing a stronger linkage between integrin-mediated signaling and skeletal muscle hypertrophy; however, there appears to be abundant justification for this type of research.

overload; Rho signaling; focal adhesion kinase signaling


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