one characteristic of diabetic nephropathy although it also involves other cells in interaction including podocytes and endothelial cells. Mesangial expansion occurs due to increased deposition of extracellular matrix proteins, for example fibronectin, into the mesangium. Accumulation of extracellular matrix proteins then occurs due to insufficient degradation by matrix metalloproteinases. Increased glucose levels results in the activation of metabolic pathways leading to increased oxidative stress. This in turn results in the over-production and accumulation of advanced glycosylation end products responsible for enhancing the risk of developing glomerular diseases. Mesangial cells grown on advanced glycosylation end product-modified matrix proteins demonstrate increased production of fibronectin and a decrease in proliferation. These factors eventually lead to the thickening of the glomerular basement membrane, mesangial matrix expansion then glomerulosclerosis and fibrosis. Mesangial pathologies may also develop during the early phase of diabetes. Glomerular hypertension causes mesangial cells to stretch which causes induced expression of GLUT1 leading to increased cellular glucose. The repetition of stretching and relaxation cycle of mesangial cells due to hypertension increases mesangial cell proliferation and the production of extracellular matrix which can then accumulate and lead to glomerular disease. See also List of human cell types derived from the germ layers References Cell biology