Journal
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 6
Volume 6, Issue -, Pages 395-423Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pathol.4.110807.092150
Keywords
hyperglycemia; advanced glycation products; protein kinase C; GTP-binding proteins; reactive oxygen species; hypertension; tubulointerstitial fibrosis
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK028492, R01DK060635, R37DK028492, R01DK044513] Funding Source: NIH RePORTER
- NIDDK NIH HHS [R01 DK044513, R01 DK028492, DK44513, DK28492, R37 DK028492, R01 DK060635, DK60635] Funding Source: Medline
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Diabetic nephropathy is a well-known complication of diabetes and is a leading cause of chronic renal failure in the Western world. It is characterized by the accumulation of extracellular matrix in the glomerular and tubulointerstitial compartments and by the thickening and hyalinization of intrarenal vasculature. The various cellular events and signaling pathways activated during diabetic nephropathy may be similar in different cell types. Such cellular events include excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products, activation of protein kinase C, increased expression of transforming growth factor beta and GTP-binding proteins, and generation of reactive oxygen species. In addition to these metabolic and biochemical derangements, changes in the intraglomerular hemodynamics, modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-induced injury. Events involving various intersecting pathways occur in most cell types of the kidney.
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