Lukic Ivan K, Humpert Per M, Nawroth Peter P, Bierhaus Angelika
Department of Medicine I and Clinical Chemistry, University of Heidelberg, Heidelberg, Germany.
Ann N Y Acad Sci. 2008 Apr;1126:76-80. doi: 10.1196/annals.1433.059.
The molecular mechanisms underlying loss of pain perception in diabetic neuropathy are poorly understood. Experimental diabetic neuropathy models recently provided evidence that engagement of the receptor for advanced glycation end products (RAGE) and RAGE-dependent sustained activation of the proinflammatory transcription factor nuclear factor kappa B might significantly contribute to reduced nociception. Most importantly, diabetes-induced loss of pain perception is largely prevented in RAGE-deficient mice compared to RAGE-bearing wild-type mice. Identifying RAGE-dependent inflammation as one pathomechanism underlying neuronal dysfunction might provide the basis for new therapeutic approaches.
糖尿病性神经病变中痛觉丧失的分子机制尚不清楚。实验性糖尿病性神经病变模型最近提供了证据，表明晚期糖基化终末产物受体（RAGE）的激活以及RAGE依赖的促炎转录因子核因子κB的持续激活可能显著导致痛觉降低。最重要的是，与野生型RAGE小鼠相比，RAGE基因缺陷小鼠在很大程度上预防了糖尿病引起的痛觉丧失。将RAGE依赖的炎症确定为神经元功能障碍的一种发病机制，可能为新的治疗方法提供依据。
