Figure 4.

Pathways in muscle catabolism in cancer CAS. Under normal physiological conditions, anabolic (green) and catabolic (red) muscle metabolic signaling pathways are balanced via reciprocal control of the protein kinase AKT, SMAD, and forkhead family transcription factors (FOXO), and muscle mass remains constant. Muscle wasting in cancer CAS is mediated by decreased host insulin-like growth factor-1 (IGF-1) and increased levels of circulating cytokines including prostaglandins, tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). The ensuing mitochondrial dysfunction, autophagy, and apoptosis result in muscle degradation and wasting. Whilst several targeting agents are available, their efficacy in cancer CAS remains to be determined. For more details refer to the text (Adapted from Argiles et al. [12]).