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The podocyte: A potential therapeutic target in diabetic nephropathy?

Lookup NU author(s): Emerita Professor Sally Marshall


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Over the last five years, much work has underlined the important role of the podocyte in the development of diabetic nephropathy. The metabolic and haemodynamic abnormalities of the diabetic milieu act in concert, perhaps via the common effector path of oxidative stress and development of reactive oxygen species, to promote podocyte damage. There is loss of nephrin from the slit diaphragm, increased synthesis of some of the components of the glomerular basement membrane, activation of pro-apoptotic and hypertrophic pathways, loss of the α 3β1 integrin and increased secretion of VEGF. These changes interact to lead to increased permeability, accumulation of abnormal extracellular matrix, apoptosis, foot process detachment and podocyte loss. The foot processes of the remaining podocytes hypertrophy and widen, with reduced filtration slit width. The end result is increasing proteinuria, basement membrane thickening and accumulation of mesangial matrix and declining renal function. Some currently used therapies, such as tight glucose control and inhibition of the renin angiotensin system, ameliorate these changes and prevent podocyte loss. Statins may also have a specific podocyte protective role. Other potential therapies include inhibitors of glycation, antioxidants, and inhibitors of growth factor and signalling pathways. © 2007 Bentham Science Publishers Ltd.

Publication metadata

Author(s): Marshall SM

Publication type: Article

Publication status: Published

Journal: Current Pharmaceutical Design

Year: 2007

Volume: 13

Issue: 26

Pages: 2713-2720

ISSN (print): 1381-6128

ISSN (electronic): 1873-4286

Publisher: Bentham Science Publishers Ltd.


DOI: 10.2174/138161207781662957

PubMed id: 17897015


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