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      Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation.

      Mycobiology
      Aging, physiology, Animals, Diabetes Complications, physiopathology, Glycosylation End Products, Advanced, Humans, Inflammation, Mice, Neurodegenerative Diseases, Oxidative Stress, Receptors, Immunologic

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          Abstract

          The products of nonenzymatic glycation and oxidation of proteins and lipids, the advanced glycation end products (AGEs), accumulate in a wide variety of environments. AGEs may be generated rapidly or over long times stimulated by a range of distinct triggering mechanisms, thereby accounting for their roles in multiple settings and disease states. A critical property of AGEs is their ability to activate receptor for advanced glycation end products (RAGE), a signal transduction receptor of the immunoglobulin superfamily. It is our hypothesis that due to such interaction, AGEs impart a potent impact in tissues, stimulating processes linked to inflammation and its consequences. We hypothesize that AGEs cause perturbation in a diverse group of diseases, such as diabetes, inflammation, neurodegeneration, and aging. Thus, we propose that targeting this pathway may represent a logical step in the prevention/treatment of the sequelae of these disorders.

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