Mechanism of fibrosis

John Varga*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations

Abstract

Fibrosis is characterized by replacement of normal tissue architecture with stiff collagen-rich connective tissue. Fibrosis is the hallmark of scleroderma, as well as a large and heterogeneous group of human diseases. In these conditions, fibrosis represents the end result of a complex series of vascular and immune-mediated responses to injury in a genetically predisposed individual [1]. As illustrated in Fig. 21.1, injured or activated vascular, epithelial and immune cells produce soluble mediators, autoantibodies and reactive oxygen species (ROS) that induce the activation and differentiation of mesenchymal cells, leading to excessive matrix deposition and increasing stiffness and ultimately irreversible remodeling, and fibrosis.

Original languageEnglish (US)
Title of host publicationScleroderma
Subtitle of host publicationFrom Pathogenesis to Comprehensive Management
PublisherSpringer US
Pages255-265
Number of pages11
ISBN (Electronic)9781441957740
ISBN (Print)9781441957733
DOIs
StatePublished - Jan 1 2012

Keywords

  • Collagen
  • Cytokine
  • Egr-1
  • Fibroblast
  • Fibrosis
  • Matrix
  • Myofibroblast
  • Pericyte
  • Smad
  • TGF-β

ASJC Scopus subject areas

  • Medicine(all)

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