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Reactive oxygen species production in acute hypoxia: oxygen sensing by mitochondrial complex I and the role of the sodium/calcium exchanger NCLX

AuthorsHernansanz-Agustín, Pablo; Ramos, Edurne; Navarro, Elisa; Parada, Esther; Moreno, Laura; Izquierdo-Álvarez, Alicia; Buendía Abaitua, Izaskun; Cogolludo, Angel; Egea Maiquez, Javier; López, Manuela G.; Martínez-Ruiz, Antonio
Issue Date2016
Citation3rd Symposium on Biomedical Research (2016)
AbstractOxygen is a key molecule of aerobic life, but can give rise to reactive oxygen species (ROS) as metabolic byproducts of oxidative phosphorylation. Acute hypoxia produces a superoxide burst, which can signal downstream cell adaptations. Here we show that hypoxia triggers acute deactivation of mitochondrial complex I, changing its catalytic activity from an oxidoreductase to a Na+/H+ antiporter. The subsequent stimulation of mitochondrial Na+/Ca2+ exchanger (NCLX) activity promotes mitochondrial depolarization and superoxide production and underlies the participation of both complex I and NCLX in acute oxygen sensing. NCLX inhibition is associated with the suppression of downstream ROS-driven responses to hypoxia such as hypoxic pulmonary vasoconstriction, HIF-1α stabilization and ischemic brain damage in vivo. These results provide biological explanations for superoxide production in acute hypoxia and highlight complex I and NCLX as potential therapeutic targets in diseases involving mitochondrial ROS signalling, hypoxia and oxidative stress.
DescriptionResumen del póster presentado al 3rd Symposium on Biomedical Research: "Advances and Perspectives in Neuroscience", celebrado en la Universidad Autónoma de Madrid el 22 de abril de 2016.-- et al.
Appears in Collections:(IIBM) Comunicaciones congresos
(CBM) Comunicaciones congresos
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