Recently visual impairment in adults due to hyperglycemia is primarily attributed to Type 2 Diabetic Retinopathy. Type 2 Diabetic Retinopathy is the end result of hyperglycemia which leads to separation of the retina causing blindness. Epigenetic alteration in disease development is attributed to the interaction between genetic and environmental factors. For the pathogenesis of Type 2 Diabetic retinopathy epigenetic changes can play a major role. Recent studies shows that through the TrkB/ERK/MAPK pathway BDNF can protect retinal neurons from hyperglycemia and also provides novel insights into the pathogenesis of Type 2 Diabetic Retinopathy. It is formulated that increased level of glucose may inhibit the conversion of DNA methylation (5mC) to hydroxymethylation (5hmC) by the ten-eleven translocation (TET) dioxygenases family of proteins by influencing α-ketoglutarate levels. Under this hypothesis, increased level of blood glucose would increase 5hmC levels due to elevated TET activity, which in turn would deregulate gene expression. The main outlook of this review is the regulation of hypermethylation by epigenetic changes of TET protein-mediated in DNA methylation/ demethylation in BDNF for a detailed insight into the pathogenesis of Type 2 Diabetic retinopathy.

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