Emilio Fernández

TL;DR: By actively downregulating glycolysis by APC/C–Cdh1, neurons use glucose to maintain their antioxidant status at the expense of its utilization for bioenergetic purposes.

TL;DR: A lentiviral reporter system is developed to assay longitudinal changes in cell signaling and transcription factor activity in living cells throughout iPSC reprogramming of human dermal fibroblasts and shows that an early burst in oxidative phosphorylation and elevated reactive oxygen species generation mediates increased NRF2 activity, which initiates the HIFα-mediated glycolytic shift and may modulate glucose redistribution to the pentose phosphate pathway.

TL;DR: Results reveal that, by inhibition of APCCdh1, glutamate receptors activation stabilizes PFKFB3 thus switching neuronal metabolism leading to oxidative damage and neurodegeneration.

TL;DR: Astrocytic mitochondrial ROS regulate glucose utilization via the pentose-phosphate pathway and glutathione metabolism, which modulates the redox status and potentially the survival of neurons, and demonstrate that mitochondrial ROS are important regulators of organismal physiology in vivo.

TL;DR: A pro-inflammatory stimulus like IL1β transforms excess glucose into a vascular deleterious agent by causing an increase in glucose uptake and its subsequent diversion into the PPP, promoting the pro-oxidant conditions required for the exacerbation of pro- oxidant and pro- inflammatory pathways.