Pleiotropy of tumor necrosis factor-α in C2C12 myotubes: in vitro studies on genes, networks and pathways involved in TNF-α induced skeletal muscle atrophy

Background Skeletal muscle atrophy is one of the most common phenomenon occurring in a variety of conditions that range from muscular inactivity to disease states such as diabetes, and cancer. Activation of inflammatory pathways by various cytokines is one of the critical events leading to skeletal muscle atrophy. Though there is significant literature on the role that the cytokine, tumor necrosis factor-a (TNF-a) plays in the induction of nuclear factor-kappa B (NFB) and ubiquitin-proteasome pathways, the molecular mechanisms involved in TNF-a induced skeletal muscle wasting remain poorly understood. Understanding how TNF-a regulates the expression/activation of various gene networks and pathways is essential not only to understand the disease prognosis but also to obtain a better molecular insight in skeletal muscle development and wasting.