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Fig. 7. A schematic representation of the proposed mechanism by which high glucose, via its effect on peroxynitrite, inactivates the VEGF/PI 3-kinase/Akt-1 pro-survival pathway and stimulates cell death via activation of p38 MAP kinase pathway. Nitration of PI 3-kinase is proposed as a mechanism by which high glucose switches off the VEGF pro-survival pathway and triggers the pro-apoptotic pathway.





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