Pathogenic Role of TGF- β in Diabetic NephropathyHyun Soon Lee*
Renal Pathology Laboratory, Hankook Kidney and Diabetes Institute, Korea
- *Corresponding Author:
- Hyun Soon Lee
Renal Pathology Laboratory
Hankook Kidney and Diabetes Institute
Songpa-gu, Samhaksaro 93, Seoul, Korea, 138-840
E-mail: [email protected]
Received date May 24, 2013; Accepted date June 30, 2013; Published date July 05, 2013
Citation: Lee HS (2013) Pathogenic Role of TGF- β in Diabetic Nephropathy. J Diabetes Metab S9:008. doi:10.4172/2155-6156.S9-008
Copyright: © 2013 Lee HS. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
About one-third of diabetic patients develop diabetic kidney disease. In renal cells, transforming growth factor- β (TGF-β) is a key regulator of extracellular matrix protein synthesis and is secreted as latent complexes. Chronic hyperglycemia in diabetic patients seems to stimulate the glomerular mesangial cells to secrete TGF- β, which is stored in the mesangial matrix and then localized to the podocyte surface. Glomerular hypertension in the diabetic kidney may upregulate angiotensin II (Ang II) in podocytes, which may activate the latent TGF- β. Activated TGF- β /Smad signaling may stimulate the podocytes to overproduce α3(IV) collagen, leading to glomerular basement membrane (GBM) thickening. Furthermore, TGF-β-induced connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF) may stimulate mesangial cells to overproduce matrix, culminating in diabetic glomerulo sclerosis. TGF-β- induced podocyte loss may also contribute to the development of glomerulosclerosis. Together, this review provides new mechanistic insights into the renal activation of TGF-ß signaling and TGF-ß-induced glomerular pathology in diabetic nephropathy.