New insights into the mechanisms of fibrosis and sclerosis in diabetic
Authors Brosius FC
Submitted By Frank Brosius on 2/8/2009
Status Published
Journal Reviews in endocrine & metabolic disorders
Year 2008
Date Published 12/1/2008
Volume : Pages 9(4) : 245 - 254
PubMed Reference 18726161
Abstract 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
Frank BrosiusUniversity of Arizona


Ltbp1latent transforming growth factor beta binding protein 1
Nos3nitric oxide synthase 3, endothelial cell
Tgfb1transforming growth factor, beta 1