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Fig. 4 | Clinical Epigenetics

Fig. 4

From: Dysregulation of 2-oxoglutarate-dependent dioxygenases by hyperglycaemia: does this link diabetes and vascular disease?

Fig. 4

Hyperglycaemia may affect ten-eleven translocation (TET) and Jumonji C (JmjC) activity by altering Fe2+ availability. a Hyperglycaemia increases flux through the polyol pathway, which consumes reduced nicotinamide adenine dinucleotide phosphate (NADPH). Reduced glutathione (GSH) and vitamin C levels may decrease as a result, decreasing the regeneration of Fe2+ which is required by TET and JmjC enzymes. Increased generation of reactive oxygen species (ROS) in hyperglycaemia may also affect Fe2+ regeneration. b An increase in cyclic adenosine monophosphate (cAMP) levels in hyperglycaemia may increase the intracellular labile Fe2+ pool and thus increase TET and JmjC activity. Abbreviations: glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), Fructose-1,6-bisphosphate (F1,6P2), glyceraldehyde-3-phosphate (G3P), 1,3-bisphosphoglycerate (1,3 BPG)

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