The Role of Transforming Growth Factor-Beta in Diabetic Nephropathy

Figure 1

Activation of TGF-β synthesis and its role in proinflammatory mechanisms in T2D nephropathy. (a) Increased extracellular glucose levels, mesangial cell stretch, activation of renin-angiotensin system, reactive oxidant species (ROS), and advanced glycation end products (AGEs) activate TGF-β synthesis via protein kinase C. TGF-β stimulates its own pathway through autocrine or paracrine action. TGF-β assembles a receptor complex that activates Smads that regulate nuclear transcription. (b) TGF-β1 and IL-6 promote the differentiation of naive T lymphocytes into proinflammatory T helper that produces IL17 through the transcription factor IκB𝜁. The outcomes of these processes are glomerulosclerosis and interstitial fibrosis.