Mechanisms of kidney fibrosis and the role of antifibrotic therapies
Authors Leo Deelman and Kumar Sharma
Submitted By Kumar Sharma on 12/15/2008
Status Published
Journal Current opinion in nephrology and hypertension
Year 2009
Date Published 1/1/2009
Volume : Pages 18 : 85 - 90
PubMed Reference 19077695
Abstract Purpose of review
Kidney fibrosis is a common observation in human and experimental models of
kidney disease and contributes to the progressive loss of kidney function. This
review discusses the recent recognition of the role of podocytes in the
development of common glomerular disease and focuses on the basis for new
antifibrotic therapies.
Recent findings
A growing body of evidence indicates that changes in the structure and function
of podocytes are involved in the development and progression of kidney disease.
changes include podocyte de-differentiation, podocyte-mediated endothelial
dysfunction and podocyte-induced epithelial–mesenchymal transition, all
contributing to the development of kidney fibrosis. Furthermore, new
antifibrotic strategies aiming at the transforming growth factor-beta,
connective tissue growth factor, angiotensin (1–7), and advanced glycation
endproducts/receptors advanced glycation endproducts signaling pathways are
being developed.
Podocytes are recognized to play a key role in the development of kidney
fibrosis. New antifibrotic therapies are rapidly progressing toward definitive
clinical trials but will need to be tested on top of the existing therapy of
renin–angiotensin system inhibition. Novel approaches targeting podocyte
function would be a promising approach for early stages of the disease.

Investigators with authorship
Kumar SharmaUniversity of California San Diego


Ltbp1latent transforming growth factor beta binding protein 1
Tgfb1transforming growth factor, beta 1