Targeting TGF-β signaling for the treatment of fibrosis

Matrix Biol. 2018 Aug;68-69:8-27. doi: 10.1016/j.matbio.2017.12.016. Epub 2018 Jan 31.

Abstract

Transforming growth factor-β (TGF-β) is widely recognized as a core pathway of fibrosis. Inhibition of TGF-β signaling may thus offer potential for antifibrotic therapies. Long-term inhibition of TGF-β signaling at the level of its isoforms and receptors can be associated with unacceptable adverse effects. However, TGF-β regulates a myriad of intracellular signaling cascades to transmit its profibrotic effects and several of those pathways offer potential for pharmacologic intervention. Moreover, the multiple interactions of TGF-β with other profibrotic pathways also yielded candidates for therapeutic intervention. In this review, we discuss selected targets within the TGF-β pathway with high translational potential.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antibodies, Monoclonal / pharmacology
  • Antibodies, Monoclonal / therapeutic use
  • Clinical Trials as Topic
  • Fibrosis / drug therapy*
  • Fibrosis / metabolism
  • Humans
  • Receptors, Transforming Growth Factor beta / metabolism
  • Serotonin Receptor Agonists / pharmacology
  • Serotonin Receptor Agonists / therapeutic use
  • Signal Transduction / drug effects*
  • Transforming Growth Factor beta / metabolism*
  • Translational Research, Biomedical

Substances

  • Antibodies, Monoclonal
  • Receptors, Transforming Growth Factor beta
  • Serotonin Receptor Agonists
  • Transforming Growth Factor beta