Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy

Abstract

Diabetes mellitus and its complications are becoming one of the most important health problems in the world. Diabetic nephropathy is now the main cause of end-stage renal disease. The mechanisms leading to the development and progression of renal injury are not well known. Therefore, it is very important to find new pathogenic pathways to provide opportunities for early diagnosis and targets for novel treatments. At the present time, we know that activation of innate immunity with development of a chronic low grade inflammatory response is a recognized factor in the pathogenesis of diabetic nephropathy. Numerous experimental and clinical studies have shown the participation of different inflammatory molecules and pathways in the pathophysiology of this complication.

Keywords: Diabetes; Diabetic nephropathy; Inflammation; Innate immunity; Renal failure.

Figure 1

Schematic overview of the participation of inflammatory mechanisms in the pathophysiology of diabetic nephropathy. MCP: Monocyte chemoattractant protein; CSF: Colony-stimulating factor; ICAM: Intercelular adhesion molecule; VCAM: Vascular cell adhesion molecule. TGF: Transforming growth factor; CTGF: Connective tissue growth factor; VEGF: Vascular endothelial growth factor; TNF-α: Tumor necrosis factor alpha.

Figure 2

Sorbitol-aldose reductase pathway activation in diabetes mellitus. NAD: Nicotinamide adenine dinucleotide; NADPH: Nicotinamide adenine dinucleotide phosphate.