Beyond TGFβ: Novel ways to target airway and parenchymal fibrosis

C. E. Boorsma, B. G. J. Dekkers, E. M. van Dijk, K. Kumawat, J. Richardson, J. K. Burgess, A. E. John*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

13 Citations (Scopus)

Abstract

Within the lungs, fibrosis can affect both the parenchyma and the airways. Fibrosis is a hallmark pathological change in the parenchyma in patients with idiopathic pulmonary fibrosis (IPF), whilst in asthma or chronic obstructive pulmonary disease (COPD) fibrosis is a component of the remodelling of the airways. In the past decade, significant advances have been made in understanding the disease behaviour and pathogenesis of parenchymal and airway fibrosis and as a result a variety of novel therapeutic targets for slowing or preventing progression of these fibrotic changes have been identified. This review highlights a number of these targets and discusses the potential for treating parenchymal or airway fibrosis through these mediators/pathways in the future.

Original languageEnglish
Pages (from-to)166-180
Number of pages15
JournalPulmonary Pharmacology & Therapeutics
Volume29
Issue number2
DOIs
Publication statusPublished - Dec-2014

Keywords

  • Fibrosis
  • Airway
  • Parenchyma
  • IPF
  • COPD
  • Asthma
  • IDIOPATHIC PULMONARY-FIBROSIS
  • TISSUE GROWTH-FACTOR
  • INDUCED LUNG FIBROSIS
  • SMOOTH-MUSCLE-CELLS
  • WNT1-INDUCIBLE SIGNALING PROTEIN-1
  • EPITHELIAL-MESENCHYMAL TRANSITION
  • EXTRACELLULAR-MATRIX PRODUCTION
  • PROTEASE-ACTIVATED RECEPTOR-1
  • ANGIOTENSIN-II
  • TRANSFORMING GROWTH-FACTOR-BETA-1

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