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. Author manuscript; available in PMC: 2011 Oct 29.
Published in final edited form as: Circ Res. 2010 Oct 29;107(9):1058–1070. doi: 10.1161/CIRCRESAHA.110.223545

Fig 2.

Fig 2

Model of ischemia-induced neovascularization in normal and high glucose. A. In the presence of normal glucose concentration, ischemia-stabilized HIF1α forms heterodimers with ARNT which bind the coactivator p300. This complex binds to the hypoxia response element (HRE) and activates expression of genes required for neovascularization. B. High glucose-induced methylglyoxal (MG) modifies HIF1α and p300, inhibiting complex binding to the HREs of genes required for neovascularization (Data from Thangarajah et al. [34] and Ceradini, et al.[35]) (Illustration Credit: Ben Smith/Cosmocyte)