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Chapter category: Extracellular Matrix

Molecular Developments in the Treatment of Renal Fibrosis

This chapter appears in the following book:

Fibrogenesis: Cellular and Molecular Basis

Edited by: Mohammed Shawkat Razzaque
ISBN: 0-306-47861-7
» Get more information about this book at landesbioscience.com «

Chapter authors:
Gavin J. Becker and Tim D. Hewitson

Progressive renal disease is associated with the development of fibrosing lesions not only in the glomerulus, but also in the interstitial and vascular compartments of the kidney, in a process that involves the mesenchymally derived, phenotypically similar, mesangial cell, myofibroblast and vascular smooth muscle cell. The similarities in the pathogenesis of all three processes means that the search for rational treatment strategies for any one may be of universal benefit to the others. Potential therapeutic strategies target fibrosis both indirectly and directly. Indirect therapies alter the environment the kidney operates in such as by controlling blood pressure, hyperlipidemia and hyperglycaemia. As our understanding of the mechanisms of fibrosis increase, we are developing more direct treatment strategies that target the vasoactive mediators, growth factors and cell signaling pathways that regulate renal fibrogenesis. Finally attempts to increase collagen degradation and maintain blood supply are likely to reduce the damage resulting from aberrant collagen synthesis.

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