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The potential relation between oxidative stress and the "metabolic memory" is presently the most discussed hypothesis [ 13].

The metabolic memory is linked not only to AGEs-RAGE axis but also to some other pathways [ 23- 26].

The mechanisms through which metabolic memory is retained and the role of metabolic memory in DR disease development remain to be described [ 13].

It is now well established that a central mechanism underlying metabolic memory is the persistence of hyperglycemia-associated epigenetic patterns that sustain and drive the progression of disease phenotypes, despite long-term normalization of glycemic control.

Identification of genes in our epigenetic profile that are linked to angiogenesis, ECM production and myofibril contraction indicate that hyperglycemia-driven, metabolic memory is targeting functions critical to wound healing.

It is thought that metabolic memory is the result of long-term molecular changes, such as flux through the polyol and hexosamine pathways and activation of protein kinase C [ 18], as well as oxidative and nitrosative stress [ 19].

The mechanisms of metabolic memory are poorly understood, but various genetic and epigenetic influences have been suggested.

The concept of metabolic memory was first described among patients with type 1 diabetes in 2005, based on the results of the follow-up observation of the original cohort in the DCCT [ 1].

This effect is referred to as glycemic (or metabolic) memory and is responsible for various complications in the treatment of diabetic patients.

Differences in DNA methylation detected after prolonged culture of these diabetic, patient-derived fibroblast cell lines in normoglycemic conditions strongly suggest retained metabolic memory that is associated with poor wound healing outcomes in these diabetic patients.

Based on the results of recent randomized, controlled clinical trials and analyses of their follow-up periods the concept of metabolic memory cannot be restricted to antihyperglycaemic treatment only, rather it can be extended to lipid-lowering and antihypertensive treatment and even life-style modification.