Conclusion

Multiple mechanisms are involved in the pathogenesis of PDN. New findings support the role for previously discovered mechanisms, such as increased AR activity, nonen-zymatic glycation, PKC activation, and oxidative stress in functional and morphological abnormalities in the diabetic nerve. Evidence for the important role for nitrosative stress, MAPK activation, PARP activation, COX-2 activation, and Ca2+ signaling is emerging. Several newly discovered mechanisms include activations of NF-kB, the 12/15-LO pathway, and NHE-1. Studies of the role for these mechanisms in PDN and their interactions with other pathogenetic factors are in progress.

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