Extracellular matrix degradation in liver fibrosis: Biochemistry and regulation

John P. Iredale*, Alexandra Thompson, Neil C. Henderson

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

Abstract

Fibrosis is a highly conserved wound healing response and represents the final common pathway of virtually all chronic inflammatory injuries. Over the past 3 decades detailed analysis of hepatic extracellular matrix synthesis and degradation using approaches incorporating human disease, experimental animal models and cell culture have highlighted the extraordinarily dynamic nature of tissue repair and remodelling in this solid organ. Furthermore emerging studies of fibrosis in other organs demonstrate that basic common mechanisms exist, suggesting that bidirectionality of the fibrotic process may not solely be the preserve of the liver. In this review we will examine the cellular and molecular mechanisms that govern extracellular matrix degradation and fibrosis resolution, and highlight how manipulation of these processes may result in the development of effective anti-fibrotic therapies. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease. (C) 2012 Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)876-883
Number of pages8
JournalBBA - Molecular Basis of Disease
Volume1832
Issue number7
DOIs
Publication statusPublished - Jul 2013

Keywords

  • Fibrosis
  • Matrix
  • Metalloproteinase
  • Macrophage
  • Hepatic stellate cell
  • HEPATIC STELLATE CELLS
  • NORMAL RAT-LIVER
  • FAT-STORING CELLS
  • TISSUE INHIBITOR
  • MESENCHYMAL TRANSITION
  • LIPOCYTES SYNTHESIZE
  • COLLAGENASE ACTIVITY
  • TRANSGENIC MOUSE
  • GENE-EXPRESSION
  • PRIMARY CULTURE

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