title: Reactive oxygen species and calcium signals in skeletal muscle: A crosstalk involved in both normal signaling and disease.
abstract: Reactive Oxygen Species (ROS) have been profusely studied as agents of potential damage to living cells and they have been related to a number of pathological processes. Increasing evidence points to a more positive role of ROS in cell signaling and the detailed mechanism that regulates the precise amount of ROS needed for cell functioning without the deleterious effects of excess ROS still needs to be resolved in detail. In skeletal muscle the main source of ROS during normal functioning appears to be NADPH oxidase 2 (NOX2), which is activated by electrical stimuli (or exercise) through a cascade of events that include ATP release through pannexin1 channels. NOX2 is a protein complex that assembles in the T-tubule membrane before activation and ROS production by NOX2 appears to be important for muscle adaptation through gene expression and mitochondrial biogenesis as well as for improving glucose transport after insulin action. Excess ROS production (or diminished antioxidant defenses) plays a role in a number of pathological processes in skeletal muscle. Together with increased reactive nitrogen species, an increase in ROS appears to have a deleterious role in a model of Duchenne muscular dystrophy as well as muscle wasting in other diseases such as aging sarcopenia and cancer cachexia. In addition, ROS is involved in obesity and muscle insulin resistance, both of which are causally related to type 2 diabetes. A detailed description of the fine-tuning of ROS (including all sources of ROS) in skeletal muscle in health and disease will significantly contribute to our knowledge of both muscle adaptation and muscle related pathologies.
authors.affiliation: Departamento de Tecnología Médica, Facultad de Medicina, Universidad de Chile, Independencia 1027, 8380453 Santiago, Chile.
authors.forename: Alejandra
authors.initials: A
authors.lastname: Espinosa
authors.affiliation: Centro de Estudios Moleculares de la Célula, ICBM, Facultad de Medicina, Universidad de Chile, Chile; Unidad de Fisiología Integrativa, Laboratorio Ciencias del Ejercicio, Clínica MEDS, Las Condes, Chile.
authors.forename: Carlos
authors.initials: C
authors.lastname: Henríquez-Olguín
authors.affiliation: Centro de Estudios Moleculares de la Célula, ICBM, Facultad de Medicina, Universidad de Chile, Chile. Electronic address: ejaimovi@med.uchile.cl.
authors.forename: Enrique
authors.initials: E
authors.lastname: Jaimovich
mesh_terms: D000818:Animals; D020013:Calcium Signaling; D004194:Disease; D006801:Humans; D008954:Models, Biological; D018482:Muscle, Skeletal / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015290:Second Messenger Systems
chemical_list: D017382:Reactive Oxygen Species
keywords: Inflammation; Muscle wasting; Muscular dystrophy; NADPH oxidase; Obesity; Sarcopenia; Type 2 diabetes