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Reversal of Cardiac Fibrosis and Related Dysfunction by Relaxin
Author(s) -
Du XiaoJun,
Xu Qi,
Lekgabe Edna,
Gao XiaoMing,
Kiriazis Helen,
Moore XiaoLei,
Dart Anthony M.,
Tregear Geoffrey W.,
Bathgate Ross A. D.,
Samuel Chrishan S.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2008.03780.x
Subject(s) - relaxin , medicine , fibrosis , cardiac fibrosis , heart failure , myocardial fibrosis , myocardial infarction , cardiology , bioinformatics , hormone , biology
As a hallmark of heart disease, cardiac fibrosis contributes to the development of heart failure and arrhythmias and forms a key therapeutic target. There is a major unmet need for selective, potent, and safe antifibrotic drugs. Earlier studies revealed a cardiac fibrosis phenotype in relaxin‐1‐deficient mice. Recent studies in several rodent models of cardiac fibrosis have documented reversal of fibrosis by treatment with relaxin peptide or virally mediated relaxin gene delivery. In mice with surgically induced transmural myocardial infarction, relaxin therapy inhibited scar density. In these studies, however, functional benefits achieved by relaxin therapy were limited or less explored. Collectively, there is good experimental evidence that relaxin is able to reverse cardiac fibrosis due to distinct mechanisms. Future research needs to explore functional improvement following fibrosis reversal by relaxin and the usefulness of relaxin in antiarrhythmic or stem cell‐based therapy.