摘要

Various pathological conditions can induce skeletal muscle atrophy due to the fact that rates of protein degradation exceed rates of protein synthesis. Common examples in the field of intensive care medicine are critical illness myopathy and critical illness polyneuropathy. In these catabolic states, the atrogins MuRF1 (Muscle specific ring finger protein 1) and MAFbx are upregulated. These genes encode for two ubiquitin ligases which mediate the ubiquitination of myofibrillar and other proteins and their subsequent degradation in the ubiquitin-proteasome system (UPS). The present article examines molecular mechanisms and the possible clinical relevance of MuRF1 and MAFbx.

  • 出版日期2009-4