Targeting GPCR Signaling for Idiopathic Pulmonary Fibrosis Therapies

Andrew J. Haak, Merrick T. Ducharme, Ana M. Diaz Espinosa, Daniel J. Tschumperlin

Research output: Contribution to journalReview article

3 Scopus citations

Abstract

A variety of G protein-coupled receptors (GPCRs) have been implicated in the pathogenesis of pulmonary fibrosis, largely through their promotion of profibrotic fibroblast activation. By contrast, recent work has highlighted the beneficial effects of Gαs-coupled GPCRs on reducing fibroblast activation and fibrosis. This review highlights how fibrosis-promoting and -inhibiting GPCR signaling converges on downstream signaling and transcriptional effectors, and how the diversity and dynamics of GPCR expression challenge efforts to identify effective therapies for idiopathic pulmonary fibrosis (IPF). Next-generation strategies to overcome these challenges, focusing on target selection, polypharmacology, and personalized medicine approaches, are discussed as a path towards more effective GPCR-targeted therapies for pulmonary fibrosis.

Original languageEnglish (US)
Pages (from-to)172-182
Number of pages11
JournalTrends in Pharmacological Sciences
Volume41
Issue number3
DOIs
StatePublished - Mar 2020

Keywords

  • fibrosis
  • G protein-coupled receptor
  • MRTF
  • ROCK
  • TAZ
  • YAP

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

Fingerprint Dive into the research topics of 'Targeting GPCR Signaling for Idiopathic Pulmonary Fibrosis Therapies'. Together they form a unique fingerprint.

  • Cite this