Advanced glycation irreversibly and progressively modifies proteins over time and yields the advanced glycation end-products (AGE). AGEs are thought to contribute to the development of atherosclerosis and of diabetic and uremic complications. Their inhibition has thus become a therapeutic goal. In this article, we discuss the role of various reactive carbonyl compound (RCOs) in the genesis of AGEs, postulate the existence of “carbonyl stress” in complicated diabetes and, finally, discuss therapeutic perspectives.
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