Generation of reactive oxygen species (ROS) is a ubiquitous phenomenon in eukaryotic cells' life. Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not merely toxic species but also—within certain concentrations—useful signaling molecules regulating physiological processes. During intense skeletal muscle contractile activity myotubes' mitochondria generate high ROS flows: this renders skeletal muscle a tissue where ROS hold a particular relevance. According to their hormetic nature, in muscles ROS may trigger different signaling pathways leading to diverging responses, from adaptation to cell death. Whether a “positive” or “negative” response will prevail depends on many variables such as, among others, the site of ROS production, the persistence of ROS flow or target cells' antioxidant status. In this light, a specific threshold of physiological ROS concentrations above which ROS exert negative, toxic effects is hard to determine, and the concept of “physiologically compatible” levels of ROS would better fit with such a dynamic scenario. In this review these concepts will be discussed along with the most relevant signaling pathways triggered and/or affected by ROS in skeletal muscle. 1. Introduction Oxidative stressors, such as reactive oxygen species (ROS), have been initially and long considered as merely deleterious species to skeletal muscle tissue. Indeed, since the 1980s abundant evidence clearly indicated that ROS play a pathogenic role in inherited muscular dystrophies [1] and have then been identified as concausal factors in various muscular diseases [2–5]. However, and thereafter, accumulating evidence indicated that ROS, at least within concentrations emerging from physiological conditions, could also play a positive role in physiologically relevant processes in muscle cells. As an example, inflammation-derived ROS play a contradictory role in muscle repair [2]: in combination with other actors such as growth factors and chemokines, ROS participate in a cascade of events leading to muscle regeneration and repair; on the contrary, the local persistence of ROS sustained by infiltrated neutrophils may cause further injury by oxidatively damaging differentiating myoblasts and myotubes thus delaying the restitutio ad integrum. Similarly, ROS generated during exercise promote mitochondriogenesis (a key factor in muscle differentiation) via peroxisome
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