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- W62045707 endingPage "41" @default.
- W62045707 startingPage "531" @default.
- W62045707 abstract "Diabetic nephropathy (DN) is the leading cause of chronic kidney failure. Moreover, DN is associated with elevated cardiovascular morbidity and mortality. DN is characterized by progressive expansion of the mesangial matrix and thickening of the glomerular basement membrane, resulting in the obliteration of glomerular capillaries. Advanced glycation endproducts (AGEs) produced as the result of hyperglycemia are known to stimulate the production of extracellular matrix (ECM) proteins, resulting in glomerulosclerosis. Exposure of cultured mesangial cells to AGEs results in a receptor-mediated upregulation of mRNA and protein secretion of type IV collagen (Col4), which is a major component of ECM. Here we review recent novel insights into the pathogenesis and diagnosis of DN, with a special emphasis on the emerging concept that diabetic glomerulosclerosis can result from activation of the signaling cascade leading to irreversible ECM overproduction. Finally, we describe signaling pathways involved in the initial change of DN and how these pathways can be manipulated for therapeutic benefit." @default.
- W62045707 created "2016-06-24" @default.
- W62045707 creator A5033052103 @default.
- W62045707 creator A5069412789 @default.
- W62045707 creator A5069467740 @default.
- W62045707 creator A5071914798 @default.
- W62045707 date "2011-04-01" @default.
- W62045707 modified "2023-09-29" @default.
- W62045707 title "Role of Smad1 in diabetic nephropathy: Molecular mechanisms and implications as a diagnostic marker." @default.
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- W62045707 doi "https://doi.org/10.14670/hh-26.531" @default.
- W62045707 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21360446" @default.
- W62045707 hasPublicationYear "2011" @default.
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