作者: Sally A. Price , Rebecca C. Burnand , David R. Tomlinson
DOI: 10.1007/978-1-59745-311-0_6
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摘要: This chapter covers the identification of mitogen-activated protein kinases as early stage transducers damaging effects glucose on peripheral nerves. They are activated by several metabolic consequences hyperglycemia, in particular oxidative stress, osmotic and advanced glycation end products. Inhibition one group kinases—the p38 group—prevents development reduced nerve conduction velocity experimental diabetes; such inhibition can also be achieved an aldose reductase inhibitor, giving explanation for mechanism underlying effect polyol pathway. The treatment is described with sonic hedgehog preventing normalising expression genes coding endoskeletal proteins, which may instrumental preserving integrity distal axon.