Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways

Hooi Hooi Ng, Matthew Shen, Chrishan S. Samuel, Jens Schlossmann, Robert G. Bennett

Research output: Contribution to journalReview article

3 Scopus citations

Abstract

Fibrosis is associated with accumulation of excess fibrillar collagen, leading to tissue dysfunction. Numerous processes, including inflammation, myofibroblast activation, and endothelial-to-mesenchymal transition, play a role in the establishment and progression of fibrosis. Relaxin is a peptide hormone with well-known antifibrotic properties that result from its action on numerous cellular targets to reduce fibrosis. Relaxin activates multiple signal transduction pathways as a mechanism to suppress inflammation and myofibroblast activation in fibrosis. In this review, the general mechanisms underlying fibrotic diseases are described, along with the current state of knowledge regarding cellular targets of relaxin. Finally, an overview is presented summarizing the signaling pathways activated by relaxin and other relaxin family peptide receptor agonists to suppress fibrosis.

Original languageEnglish (US)
Pages (from-to)59-65
Number of pages7
JournalMolecular and Cellular Endocrinology
Volume487
DOIs
StatePublished - May 1 2019

Keywords

  • Fibrosis
  • Nitric oxide
  • Relaxin
  • Relaxin family peptidereceptor
  • Relaxin family peptides
  • cGMP

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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