Nephrol Dial Transplant (2003) 18: 457-459
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Monocyte chemoattractant protein-1: does it play a role in diabetic nephropathy?
Department of Gastroenterology and Nephrology, Graduate School of Medical Science and Division of Blood Purification, Kanazawa University, Kanazawa and 1 Department of Molecular Preventive Medicine, School of Medicine, The University of Tokyo, Tokyo, Japan
Keywords: CCR2; chemokine; diabetic nephropathy; macrophage/monocyte; MCP-1; TGF-ß
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Introduction
Both metabolic and haemodynamic pathways impact on the progression of diabetic nephropathy [1,2]. Chronic hyperglycaemia, advanced glycation end (AGE) products, increase of sorbitol, activation of protein kinase C (PKC), glomerular hypertension and genetic susceptibility have been identified as risk factors in the progression of diabetic nephropathy [2]. Moreover, infiltration of the diseased kidneys by inflammatory cells such as monocytes/macrophages (M
) is a hallmark of diabetic nephropathy [3,4]. Infiltrated M release lysosomal enzymes, nitrous oxide (NO), reactive oxygen intermediates (ROI) and transforming growth factor (TGF)-ß, which play an essential role in renal damage [2,5]. A chemokine, monocyte chemoattractant protein (MCP)-1, also termed monocyte chemotactic and activating factor (MCAF) or CCL2, is secreted by mononuclear cells and various non-leukocytic cells including renal resident cells. In experimental glomerulonephritis models [6–8] and human nephritis [
MCP-1/CCR2 in human diabetic nephropathy
In vitro and in vivo expression of MCP-1/CCR2 in diabetic conditions
Anti-MCP-1/CCR2 treatments: novel therapeutic intervention for diabetic nephropathy?
Concluding remarks and future directions
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