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Sara Cimini, Milena Rizzardini, Gloria Biella and Lavinia Cantoni Hypoxia causes autophagic stress and derangement of metabolic adaptation in a cell model of amyotrophic lateral sclerosis Journal of Neurochemistry 129

Version of Record online: 22 JAN 2014 | DOI: 10.1111/jnc.12642

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Hypoxia activates autophagy and modifies glycolysis and mitochondrial respiration as fundamental cell adaptive mechanisms. This stress is closely related to amyotrophic lateral sclerosis. The recruitment of autophagy and mitochondrial dysfunction are documented in patients and models expressing mutant Cu, Zn superoxide dismutase (SOD1) protein, but their impact in the disease remains unclear. G93ASOD1 cells were more susceptible to hypoxia than wild-type SOD1 cells and showed autophagic stress and inappropriate handling of energy metabolism. Defective adaptation to hypoxia may contribute to neurodegeneration.

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