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Diabetic Nephropathy (DNP) is a chronic disease caused by diabetes that leads to end stage renal diseases. Although various pathological mechanisms have been proposed till date on the progression of DNP, the exact cause of this disease is still unknown. Here, we have focused on the modifications of low density lipoproteins (LDL) and its pathogenicity in DNP. LDL modification, specifically oxidation plays a major role in various disease states such as atherosclerosis, endothelial dysfunction, and cardiovascular diseases. However, its role in DNP is still unexplored. This review depicts the pathway in which LDL modification influences the development and perpetuation of DNP. Ox-LDL is taken up by the scavenger receptors such as CXCL-16 in podocytes and CD36 in tubular epithelial cells. This activates TGF-beta, which up-regulates the expression of matrix components such as collagen, fibronectin and laminin causing mesangial expansion and glomerulosclerosis. Simultaneously, there is an increased expression of VEGF and PDGF which could mediate macrophage infiltration and podocyte loss. This shows that Ox-LDL plays a major role in inducing the pathological changes in DNP.