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Diabetes is a metabolic disorder characterised by chronic hyperglycaemia, hypertension, dyslipidaemia, microalbuminuria and inflammation. Moreover, there are a number of vascular complications associated with this condition including retinopathy, neuropathy and nephropathy. Diabetic nephropathy is the major cause of end-stage renal disease in Western societies affecting a substantial proportion (25-40%) of patients with diabetes. Diabetic nephropathy is defined as a progressive decline in glomerular filtration rate, accompanied by proteinuria and other end-organ complications such as retinopathy. It is widely accepted, that diabetic nephropathy is the product of hemodynamic and metabolic factors which act in concert and drive its development and progression. Metabolic factors include hyperglycaemia, hyperlipidaemia and advanced glycation. Hemodynamic factors include alterations in flow and pressure and the activation of the Renin-Angiotensin system (RAS). Together, the hemodynamic and metabolic factors activate common downstream signalling pathways, which potentiate the activation of target growth factors and signalling pathways which likely drive the development of DN. At present the most effective therapeutics for the treatment of DN target the renin-angiotensin system. Unfortunately, whilst they slow down the progression of DN they do not prevent it and thus novel therapeutics and potential targets required. In recent times the downstream intracellular signalling pathways and their modulators have been central focus for the investigation of novel therapeutic targets for the treatment of DN. These targets include advanced glycation end products (AGEs) and their receptors, glucose transport molecules, NFB, ROS, PKC, inflammatory molecules, including adipokines, chemokines, adhesion molecules and pro-inflammatory cytokines. Moreover, pro-fibrotic molecules , including EGF, VEGF, CTGF and arguably the most important, TGF-┚, which are known to potentiate the morphological alterations associated with DN have also been targeted. Recently, epigenetic alterations, including histone, DNA methylation, metabolic memory and microRNA’s have demonstrated their potential as novel therapeutic targets in

Diabetic Nephropathy: Current and Novel Therapeutic Approaches to Prevent Its Development and Progression