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Despite this, there is currently no effective cure for the tissue structural and functional damage induced by fibrosis\u2010related disorders. Relaxin meets several criteria of an effective anti\u2010fibrotic based on its specific ability to inhibit pro\u2010fibrotic cytokine and\/or growth factor\u2010mediated, but not normal\/unstimulated, fibroblast proliferation, differentiation and matrix production. Furthermore, relaxin augments matrix degradation through its ability to up\u2010regulate the release and activation of various matrix\u2010degrading matrix metalloproteinases and\/or being able to down\u2010regulate tissue inhibitor of metalloproteinase activity. Relaxin can also indirectly suppress fibrosis through its other well\u2010known (anti\u2010inflammatory, antioxidant, anti\u2010hypertrophic, anti\u2010apoptotic, angiogenic, wound healing and vasodilator) properties. This review will outline the organ\u2010specific and general anti\u2010fibrotic significance of exogenously administered relaxin and its mechanisms of action that have been documented in various non\u2010reproductive 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\u2010fibrotic actions, highlighting its potential as an emerging anti\u2010fibrotic therapeutic.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Linked Articles<\/jats:title>\n                    <jats:p>\n                      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\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v174.10\/issuetoc\">http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v174.10\/issuetoc<\/jats:ext-link>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.13529","type":"journal-article","created":{"date-parts":[[2016,6,1]],"date-time":"2016-06-01T23:39:24Z","timestamp":1464824364000},"page":"962-976","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":133,"title":["Anti\u2010fibrotic actions of relaxin"],"prefix":"10.1111","volume":"174","author":[{"given":"C S","family":"Samuel","sequence":"first","affiliation":[{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology Monash University  Melbourne Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S G","family":"Royce","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Pharmacology Monash University  Melbourne Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T D","family":"Hewitson","sequence":"additional","affiliation":[{"name":"Department of Nephrology Royal Melbourne Hospital  Melbourne Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K M","family":"Denton","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology Monash University  Melbourne Vic. 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