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This work was supported by the National Institutes of Health under award numbers 2R01HL115189, P30DK04056, UE5DK137285, and U24 DK132733, and by the National Clinician Scholars Program at the Duke Clinical and Translational Science Institute
CaMKK2 dysfunction may play an underlying role in this phenomenon as genetic deletion of Camkk2 in hippocampal neurons, myeloid cells and immortalized cell lines (HEK293 and HepG2) results in mitochondrial dysfunction that causes a similar switch in cellular energy generation from oxidative phosphorylation to glycolysis [43, 201, 202]
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El artculo separ tres preguntas: actividad redox del metal, formacin de agregados y viabilidad celular
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