Figure 1

Multiple sources of diacylglycerol (DAG), and DAG-mediated PKC activation could contribute to renal fibrosis. Overproduction of DAG causes the activation of PKC, leading to the initiation and development of diabetic nephropathy (DN). PKC (β and δ form) primarily upregulates the NFҟB gene, TGFβ1 action, VEGF, PAI, and NADHP oxidases pathway. Increased TGFβ1, collagen, fibronectin enhanced mesangial expansion, activated NFҟB induce profibrotic gene expression, and activated VEGF cause enhanced angiogenesis, and upregulated PAI reduces fibrinolysis, whereas increased NADPH oxidase provides oxidative stress to renal cells; all of these factors could contribute to the development of renal fibrosis.