Treatment Strategies for Organ Fibrosis Based on Regulation of Collagen Metabolism

概要

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Increased production of type I collagen is a common hallmark of fibrotic diseases in various organs. A dynamic balance between the production and degradation of collagen is rigorously controlled by a number of growth factors and cytokines, and a disruption of this equilibrium causes organ fibrosis. Recent advance in understanding the regulatory mechanisms responsible for collagen metabolism has made it possible to attempt treatments of organ fibrosis from the viewpoints of molecular targeting. Transforming growth factor-β (TGF-β) plays key roles not only in stimulating type I collagen gene transcription but also in inhibiting degradation of accumulated collagen by suppressing matrix metalloproteinase-1 (MMP-1) expression. Thus, a number of studies have focused on suppression of TGF-β activation and intervention of the signaling pathways of TGF-β and its intracellular mediators, Smad proteins. Several factors have been shown to antagonize the TGF-β/Smad-stimulated collagen gene expression. Finally, attempts of gene therapy are being undertaken to reverse organ fibrosis by expressing MMP-1 or hepatocyte growth factor in the fibrotic tissue.
日本結合組織学会の論文
2003-12-25