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This Article Full Text Full Text (PDF) All Versions of this Article: 296/6/F1239    most recent 90521.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Hewitson, T. D. PubMed PubMed Citation Articles by Hewitson, T. D.

REVIEW

Renal tubulointerstitial fibrosis: common but never simple

Department of Nephrology, Royal Melbourne Hospital and Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia

Submitted 28 August 2008 ; accepted in final form 7 January 2009

ABSTRACT

Regardless of etiology, all patients with chronic renal disease show a progressive decline in renal function with time. Fibrosis, so-called scarring, is a key cause of this pathophysiology. Fibrosis involves an excess accumulation of extracellular matrix (primarily composed of collagen) and usually results in loss of function when normal tissue is replaced with scar tissue. While recent major advances have led to a much better understanding of this process, many problems remain. We for instance know little about why some wounds heal and others scar and little about how many putative antifibrotic agents work. This review discusses recent advances in our understanding of the mechanisms of tubulointerstitial fibrosis, focusing on the regulation and role of the myofibroblast in this process, the role of recently recognized endogenous antifibrotic factors, controversy surrounding the effects of metalloproteinases, and the opportunities presented by new treatment strategies that abrogate and may even reverse fibrosis.

extracellular matrix; fibroblast; fibrosis; kidney; myofibroblast