Figure 1


Figure 1: Hyperglycemia-induced activation of molecular pathways associated with diabetic complications. Diabetes and associated hyperglycemia can lead to increased activation of diacylglycerol (DAG)-protein kinase C (PKC)-mitogen activated protein kinase (MAPK), oxidative stress and circulating inflammatory cells. All of these events can lead to production and increased action of various growth factors and cytokines such as transforming growth factor (TGF)-β, connective tissue growth factor (CTGF), and vascular endothelial growth factor (VEGF) as well as activation of transcription factors such as nuclear factor (NF)-κB, and therefore will lead to infiltration, accumulation, and activation of extracellular matrix proteins in renal tissues, all of which over time can induce the development of diabetic nephropathy.

Figure 1: Hyperglycemia-induced activation of molecular pathways associated with diabetic complications. Diabetes and associated hyperglycemia can lead to increased activation of diacylglycerol (DAG)-protein kinase C (PKC)-mitogen activated protein kinase (MAPK), oxidative stress and circulating inflammatory cells. All of these events can lead to production and increased action of various growth factors and cytokines such as transforming growth factor (TGF)-β, connective tissue growth factor (CTGF), and vascular endothelial growth factor (VEGF) as well as activation of transcription factors such as nuclear factor (NF)-κB, and therefore will lead to infiltration, accumulation, and activation of extracellular matrix proteins in renal tissues, all of which over time can induce the development of diabetic nephropathy.