Abstract
Introduction: Diabetic neuropathy (DN) is a major complication of diabetes, however, the molecular mechanisms underlying increased pain in early stages of the disease are yet poorly understood. We have recently demonstrated that hyperglycemia-dependent, RAGE-mediated suppression of glyoxalase-1 (GLO-1), the major cellular defence in the detoxification of methylglyoxal (MG) contributes to increased pain in early phases of diabetic neuropathy. To further define the role of the GLO-1-system in modulating pain, we have studied diabetes induced pain in wildtype (WT), RAGE-/-, an GLO-/+ mice and the effects of direct application of either GLO-1 or MG on pain perception.
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