Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways

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

doi:10.1016/j.mce.2019.01.015

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 journal › Review Article › Research › peer-review

4 Citations (Scopus)

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 language	English
Pages (from-to)	59-65
Number of pages	7
Journal	Molecular and Cellular Endocrinology
Volume	487
DOIs	https://doi.org/10.1016/j.mce.2019.01.015
Publication status	Published - 1 May 2019

Keywords

cGMP
Fibrosis
Nitric oxide
Relaxin
Relaxin family peptidereceptor
Relaxin family peptides

Access to Document

10.1016/j.mce.2019.01.015

Link to publication in Scopus

Cite this

Ng, H. H., Shen, M., Samuel, C. S., Schlossmann, J., & Bennett, R. G. (2019). Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways. Molecular and Cellular Endocrinology, 487, 59-65. https://doi.org/10.1016/j.mce.2019.01.015

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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.",

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AU - Shen, Matthew

AU - Samuel, Chrishan S.

AU - Schlossmann, Jens

AU - Bennett, Robert G.

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