Oxidative stress, mitochondrial dysfunction, and respiratory chain enzyme defects in inflammatory myopathies.

We investigated the relationship between oxidative stress and inflammatory myopathies. We searched in the current literature the role of mitochondria and respiratory chain defects as sources of oxidative stress and reactive oxygen species production that led to muscle weakness and fatigue. Different molecules and pathways contribute to redox milieu, reactive oxygen species generation, accumulation of misfolded and carbonylated proteins that lose their ability to fulfil cellular activities. Small peptides and physical techniques proved, in mice models, to reduce oxidative stress. We focused on inclusion body myositis, as a major expression of myopathy related to oxidative stress, where mitochondrial abnormalities are causative agents as well. We described the effect of physical exercise in inclusion body myositis that showed to increase strength and to reduce beta amyloid accumulation with subsequent improvement of the mitochondrial functions. We illustrated the influence of epigenetic control on the immune system by non-coding genetic material in the interaction between oxidative stress and inflammatory myopathies.