Role of Oxidative Stress as Key Regulator of Muscle Wasting during Cachexia

Figure 2

Molecular mechanisms involved in cachexia are modulated by oxidative stress. Atrophic factors can generate oxidative stress in skeletal muscle by the activation of different sources of reactive oxygen species, such as the mitochondria, xanthine oxidase (XO), and NADPH oxidase complex with Nox subunit, in addition to the decrease in antioxidant species. Oxidative stress is able to produce mitochondrial dysfunction, increase ubiquitin proteasome system activity, increase myonuclear apoptosis, decrease the protein synthesis pathway, and deregulate autophagy, all of which are involved in cachexia-skeletal muscle atrophy.