Type-2 diabetic nephropathy is one of the major long-term microvascular complications and is the major cause of morbidity and premature mortality in individuals with type-2 diabetes mellitus. The pathogenesis of diabetic nephropathy includes both metabolic and hemodynamic factors, as well as renal hypertrophy. Hyperglycemia is necessary, but not sufficient for its initiation and progression. Diabetic nephropathy is considered to result not only from alteration of chemical composition of the glomerular basement membrane and mesangium but also from an increase in extracellular matrix accumulation due to TGF-β activation. Although large numbers of candidate genes have been analyzed, those related to initiation and progression are still obscure in patients with type-2 diabetic nephropathy. Experimental models offer the key to an understanding of this multifactorial disease.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the pathogenesis of type-2 diabetic nephropathy. We are particularly interested in articles describing the recent advances in molecular genetics, immunology, cell biology, and structural biology using experimental models. Potential topics include, but are not limited to:

• Advances in molecular genetics of type-2 diabetic nephropathy
• Role of inflammation or the autoimmune process in type-2 diabetic nephropathy
• Recent advances in structural biology in extracellular matrix
• Role of cellular dysfunction in mesangial cells and podocytes
• New cellular and animal models to test and understand the pathogenesis of type-2 diabetic nephropathy
• Current concepts in the treatment of type-2 diabetic nephropathy using small molecules, siRNA, stem cells, and viral or nonviral gene therapy strategies
• Recent clinical progress, especially treatment

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