Abstract
We examined reactive oxygen species as upstream activators of nuclear factor kappaB; (NF-kappaB) and forkhead box O (Foxo) in skeletal muscle during disuse atrophy. Catalase, an enzyme that degrades H2O2, was overexpressed in soleus muscles via plasmid injection prior to 7 days of hindlimb immobilization. The increased catalase activity abolished immobilization-induced transactivation of both NF-kappaB and Foxo and attenuated the loss of muscle mass. Thus, H2O2 may be an important initiator of these signaling pathways that lead to muscle atrophy.
