Regulation of ubiquitin-proteasome-dependent protein breakdown in experimental models in muscle atrophy

Abstract

There is more and more evidence that ATP-ubiquitin-dependent proteolytic system has a key role in muscle protein breakdown. In different experimental models in muscle atrophy we try to define factors involved in regulation of ATP-ubiquitin-dependent proteolytic pathway. If we use a simplified division, we can talk about experimental models in which we use regulation by nutrients (fasting, protein inadequate diet), by disuse of muscle (denervation, weightlessness), by pathological conditions (sepsis, acidosis, diabetes, burn injury, cachexia), by hormones (insulin, IGF-1, glucocorticoids) and by cytokines (tumor necrosis factor-a, interleukin-1, interleukin-6).