CONICET | Buscador de Institutos y Recursos Humanos

Oxidative stress can be considered a consequence ofimbalance in the formation of reactive oxygen species(ROS) and antioxidant defense systems, in which mitochondriaappear to be the main source of ROS production. A keyconcern is that high levels of ROS can modulate molecularand structural modifications and lead to functional changeswithin the muscle. In this regard, ROS causes oxidation ofbiomolecules, in which results in loss of their biologicalfunctions and leads to homeostatic imbalance. The maineffects mediated by ROS relate to its potential to cause oxidativedamage in cells and tissues [1]. Therefore, a ROS burstcontributes to cellular dysfunction and can cause a widerange of chronic diseases. Scientific advances have alloweda better understanding of the role of oxidative stress on muscularhomeostasis; thereby, deciphering and understandinghow ROS regulate specific molecules and processes that alterphysiological function could cause development of pathologies.Thus, studying the effects of ROS could assist with thedevelopment of new therapeutic avenues that address a widerange of muscle disorders.