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New insights into the mechanisms of fibrosis and sclerosis in diabetic
Frank Brosius on 2/8/2009
Reviews in endocrine & metabolic disorders
Volume : Pages
9(4) : 245 - 254
Progression of diabetic nephropathy (DN) is manifested by gradual scarring of
both the renal glomerulus and tubulointerstitial region. Over the past several
years, the general understanding of the pathogenic factors that lead to renal
fibrosis in DN has expanded considerably. In this review, some of the important
factors that appear to be involved in driving this fibrosing process are
discussed, with special emphasis on newer findings and insights. It is now clear
that multiple cell types in the kidney contribute to progressive fibrosis in DN.
New concepts about bradykinin, TGF-beta and eNOS signaling as well as JAK/STAT
activation and the central role of inflammation in both glomerular and
tubulointerstitial fibrosis are discussed.
Investigators with authorship
University of Arizona
Neuropathy & Neurocognition
latent transforming growth factor beta binding protein 1
nitric oxide synthase 3, endothelial cell
transforming growth factor, beta 1
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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