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

James A. Carson, Lei Wei

Research output: Contribution to journalReview article

89 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)337-343
Number of pages7
JournalJournal of Applied Physiology
Issue number1
StatePublished - Jan 2000


  • Focal adhesion kinase signaling
  • Overload
  • Rho signaling

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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