The JDRF Center for Type 1 Diabetes at Columbia University: Receptor for AGE (RAGE) and the Inflammatory Response: Implications for the Complications of Type 1 Diabetes - Mechanisms and Clinical Trials

Our research in experimental and clinical diabetes indicates that glucose-mediated cellular oxidative stress is a unifying mechanism underlying the microvascular complications of diabetes. Treatment strategies that halt oxidative stress decrease cell injury and, in many cases, restore function in cell culture and animal models of diabetic complications. Oxidative stress therefore is a therapeutic target in the treatment of diabetic complications. Therapies may be designed to block: 1. The initial phase of glucose-induced oxidative stress. 2. The free radicals that are generated by oxidative stress. 3. The cellular damage produced by the accumulation of free radicals. Two translational scientific projects are included in our Center, each focused on new therapeutic targets for the treatment of neuropathy. The current translational project employs botanicals to activate the natural antioxidant response in neurons affected by diabetes. This results in improved nerve structure, function and ameliorates the progression of diabetic neuropathy. A third project translates the scientific basic findings into clinical trials. The work of the projects is supported by three scientific and one administrative Core.