Study provides the first evidence of a direct relationship between the depression of protein synthesis in skeletal muscle by PIF and Ang II, through activation of PKR, and eIF2{alpha} phosphorylation, and the enhanced degradation of the myofibrillar protein myosin, through activation of NF-{kappa}B resulting in an increased expression and activity of the ubiquitin-proteasome proteolytic pathway. This suggests that agents that target PKR may be effective in the treatment of muscle atrophy in cancer cachexia or other wasting conditions.