TGFβ signaling and the control of myofibroblast differentiation: Implications for chronic inflammatory disorders

J Cell Physiol. 2018 Jan;233(1):98-106. doi: 10.1002/jcp.25879. Epub 2017 May 15.

Abstract

The myofibroblast is a highly specialized cell type that plays a critical role during normal tissue wound healing, but also contributes pathologically to chronic inflammatory conditions such as fibrosis and cancer. As fibrotic conditions continue to be a major burden to the public health system, novel therapies that target the function of myofibroblasts may show promise in the clinic. The cytokine transforming growth factor β (TGFβ) is the most potent known inducer of myofibroblast differentiation and thus represents a powerful target to modify myofibroblast function during disease. This review focuses on our current understanding of the key signaling pathways activated by TGFβ during myofibroblast differentiation.

Keywords: cancer; fibroblast; fibrosis; myofibroblast; smooth muscle α-actin; transforming growth factor β.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Differentiation*
  • Cell Movement
  • Chronic Disease
  • Humans
  • Inflammation / immunology
  • Inflammation / metabolism*
  • Inflammation / pathology
  • Mitogen-Activated Protein Kinases / metabolism
  • Myofibroblasts / immunology
  • Myofibroblasts / metabolism*
  • Myofibroblasts / pathology
  • Phenotype
  • Signal Transduction
  • Transforming Growth Factor beta / metabolism*
  • rho GTP-Binding Proteins / metabolism

Substances

  • Transforming Growth Factor beta
  • Mitogen-Activated Protein Kinases
  • rho GTP-Binding Proteins