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- W1968392325 abstract "Abstract The common denominator of endothelial damage in diabetic complications is mitochondrial overproduction of reactive oxygen species (ROS). ROS partially inhibit the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase, with a subsequent increased availability of the glycolytic metabolites, fructose-6-phosphate and glyceraldehyde-3-phosphate. In contrast to previous concepts, pericyte loss may be the result of an active elimination initiated by endothelial cells. ROS formation and downstream mechanisms have been experimentally addressed by several strategies, including antioxidants and inhibitors of hyperglycemia-induced biochemical pathways. A novel way to prevent vascular damage in diabetes is to divert glycolytic intermediates into the non-oxidative branch of the pentose–phosphate pathway by activating the key enzyme transketolase. Together, in vitro data combined with animal experiments suggest that novel strategies are available for the prevention and treatment of diabetic microvascular damage." @default.
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- W1968392325 date "2004-05-01" @default.
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- W1968392325 title "Cellular crosstalk under hyperglycemic stress—the diabetic retina as a paradigm" @default.
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- W1968392325 doi "https://doi.org/10.1016/s0531-5131(03)01859-4" @default.
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