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Publication

New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy.

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
Name Institution Frank Brosius University of Arizona

Complications
All ComplicationsBioinformatics BoneCardiomyopathy CardiovascularGastro-Intestinal (GI) NephropathyNeuropathy & Neurocognition Pediatric Endocrinology Retinopathy UropathyWound Healing

Genes
Symbol Description Ltbp1 latent transforming growth factor beta binding protein 1 Nos3 nitric oxide synthase 3, endothelial cell Tgfb1 transforming growth factor, beta 1