Nephropathy is one of the major complications of diabetes which further directs to end stage renal disease.
Extensive work has been done to find out the mechanisms involved in pathogenesis of the DN. Now, many researchers
have been convinced that almost all of the molecular mediators and intracellular signaling pathways involved in progression
of diabetic nephropathy have involvement in transforming growth factor beta (TGF- β) at some stage.
In DN, hyperglycemia causes increase in the expression of TGF- β genes, TGF- β proteins and their receptors. Increased
glucose level mediates these effects through activation of polyol pathway, protein kinase C pathway, hexosamine
pathway, increases advanced glycation end products (AGE) and increases oxidative stress. Hyperglycemia also activates
the TGF- β via activation of glucose transporters (GLUT), angiotensine II and platelet derived growth factor (PDGF).
Activated TGF-β further leads to glomerular basement membrane (GBM) thickening and glomerulosclerosis through
activation of connective tissue growth factor (CDGF) and vascular endothelial growth factor (VEGF).
We have discussed the progression of hyperglycemia to DN via TGF- β, whose schematic presentation may serve as an
effective way to understand the mechanisms and to find out an effective way for the management of diabetic nephropathy.