Diabetic retinopathy is the most common microvascular complication. During the course of the disease, it is common to develop alterations in the retina as a consequence of chronic hyperglycaemia (American Diabetes Association 2014). Diabetic retinopathy is characterized by altered vascular permeability in the retina, capillary degeneration and exaggerated neovascularization. Several miRs have been found to be upregulated in the retinas of T1DM rats, including miR-146, miR-155, miR-132 and miR-21 - all of them NF-kB responsive (Kovacs et al.

2011) . NF-kB plays an important role in the early pathogenesis of DR by triggering a pro-apoptotic program in retinal pericytes (Kowluru et al. 2003). Therefore, these miRs may reinforce the hyperglycaemia-/inflammatory-mediated vascular damage in the retina. Other upregulated miRs in diabetic endothelial retinal cells are miR-17-5p, miR-18a, miR-20a, miR-21, miR-31 and miR-155, all known to be responsive to VEGF, the most important growth factor involved in diabetic retinopathy (Kovacs et al. 2011). MiR-200b, which targets VEGF-A, is downregulated in the retinas of diabetic rats, and forced overexpression of miR-200b reversed VEGF-mediated vascular permeability (McArthur et al. 2011). A recent study has suggested that the combination of serum miR-21, miR-181c and miR-1179 as biomarkers have the ability to discriminate between proliferative and non-proliferative diabetic retinopathy (Qing et al. 2014). The above evidence highlights the potential role of miRNAs in regulating the inflammatory and neovascularization processes of diabetic retinopathy and their potential early diagnostic value for proliferative disease.


Approximately half of diabetic patients develop neuropathy, consisting of peripheral nerve dysfunction that can manifest in several different forms, including sensory, focal/multifocal and autonomic neuropathies (American Diabetes Association 2014). There is a paucity of studies relating miRNAs to the development of diabetic neuropathy. A recent study suggests that hyperglycaemia downregulates miR-146a and that this is related to increased neuronal apoptosis by increasing the expression of interleukin-1 receptor-activate kinase (IRAKI) and tumour necrosis factor- associated factor 6 (TRAF6) in a mouse model of diabetic peripheral neuropathy (Wang et al. 2014a). Indeed, several polymorphisms in miR-146a, as well as miR- 128, are associated with susceptibility to diabetic neuropathy (Ciccacci et al. 2014).

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