Nat. Rev. Neurol. doi: /nrneurol

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Text 1 Biochemistry of Glucose Damage in Diabetes.

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Nat. Rev. Neurol. doi: /nrneurol

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Nat. Rev. Neurol. doi: /nrneurol

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Nat. Rev. Neurol. doi:10.1038/nrneurol.2016.201 Figure 2 Hyperglycaemia-driven Schwann cell stress and neurodegeneration Figure 2 | Hyperglycaemia-driven Schwann cell stress and neurodegeneration. Hyperglycaemia and dyslipidaemia ultimately lead to reduction of neuronal support from Schwann cells and microvessels. In Schwann cells, RAGE (receptor for advanced glycosylation end products) signalling leads to increased glucose metabolism by aldose reductase, which generates local oxidative damage, causes inflammation and drives cells to an immature phenotype. It also affects mitochondrial function, which increases oxygen consumption, and reduces production of desert hedgehog (DHH), which affects endothelial cell function. Endothelial cells also express aldose reductase, and increased polyol pathway flux activates proinflammatory and prothrombotic pathways that reduce nerve blood flow. Disruption of neuronal support by Schwann cells and the vascular system contributes to neuropathy, in conjunction with the direct effects of diabetes on neurons themselves. Gonçalves, N. P. et al. (2017) Schwann cell interactions with axons and microvessels in diabetic neuropathy Nat. Rev. Neurol. doi:10.1038/nrneurol.2016.201