Mechanotransduction in striated muscle via focal adhesion kinase

Contractile tissues demonstrate a pronounced capacity to remodel their composition in response to mechanical challenges. Descriptive evidence suggests the upstream involvement of the phosphotransfer enzyme FAK (focal adhesion kinase) in the molecular control of load-dependent muscle plasticity. Thereby FAK evolves as a myocellular transducer of mechanical signals towards downstream transcript expression in myofibres. Recent advances in somatic gene therapy now allow the exploration of the functional involvement of this enzyme in mechanotransduction in intact muscle. Mechanical factors exert a key influence on the phenotype of striated muscle Differential modulation of protein breakdown and synthesis and gene expression has been implied as a main mechanism underlying the molecular regulation of this loaddependent muscle plasticity in animal models Molecular evidence supports the involvement of two cytoskeletal-associated phosphotransfer activities in the early steps of mechanotransduction in striated muscle