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. Author manuscript; available in PMC: 2013 Jun 14.
Published in final edited form as: Prog Retin Eye Res. 2008 May 28;27(4):331–371. doi: 10.1016/j.preteyeres.2008.05.001

Figure 17.

Figure 17

A schematic representation of the proposed mechanism by which high glucose, via its effect on peroxynitrite, inactivates the VEGF/PI3K/Akt-1 pro-survival pathway and stimulates cell death via activation of p38 MAP kinase pathway. Nitration of PI3K is proposed as a mechanism by which high glucose switches off the VEGF pro-survival pathway and triggers the pro-apoptotic pathway.