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2017 ; 174
(10
): 962-976
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Anti-fibrotic actions of relaxin
#MMPMID27250825
Samuel CS
; Royce SG
; Hewitson TD
; Denton KM
; Cooney TE
; Bennett RG
Br J Pharmacol
2017[May]; 174
(10
): 962-976
PMID27250825
show ga
Fibrosis refers to the hardening or scarring of tissues that usually results from
aberrant wound healing in response to organ injury, and its manifestations in
various organs have collectively been estimated to contribute to around 45-50% of
deaths in the Western world. Despite this, there is currently no effective cure
for the tissue structural and functional damage induced by fibrosis-related
disorders. Relaxin meets several criteria of an effective anti-fibrotic based on
its specific ability to inhibit pro-fibrotic cytokine and/or growth
factor-mediated, but not normal/unstimulated, fibroblast proliferation,
differentiation and matrix production. Furthermore, relaxin augments matrix
degradation through its ability to up-regulate the release and activation of
various matrix-degrading matrix metalloproteinases and/or being able to
down-regulate tissue inhibitor of metalloproteinase activity. Relaxin can also
indirectly suppress fibrosis through its other well-known (anti-inflammatory,
antioxidant, anti-hypertrophic, anti-apoptotic, angiogenic, wound healing and
vasodilator) properties. This review will outline the organ-specific and general
anti-fibrotic significance of exogenously administered relaxin and its mechanisms
of action that have been documented in various non-reproductive organs such as
the cardiovascular system, kidney, lung, liver, skin and tendons. In addition, it
will outline the influence of sex on relaxin's anti-fibrotic actions,
highlighting its potential as an emerging anti-fibrotic therapeutic. LINKED
ARTICLES: This article is part of a themed section on Recent Progress in the
Understanding of Relaxin Family Peptides and their Receptors. To view the other
articles in this section visit
http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.10/issuetoc.
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