Reversal of cardiac fibrosis and related dysfunction by relaxin.
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.
Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, University of Melbourne, Melbourne, Australia. xiaojun.du@bakeridi.edu.au
Xiao-Jun
XJ
Du
Qi
Q
Xu
Edna
E
Lekgabe
Xiao-Ming
XM
Gao
Helen
H
Kiriazis
Xiao-Lei
XL
Moore
Anthony M
AM
Dart
Geoffrey W
GW
Tregear
Ross A D
RA
Bathgate
Chrishan S
CS
Samuel
D000818:Animals; D004195:Disease Models, Animal; D005355:Fibrosis / Q000188:drug therapy* / Q000517:prevention & control*; D006331:Heart Diseases / Q000188:drug therapy* / Q000517:prevention & control*; D006801:Humans; D051379:Mice; D051381:Rats; D012065:Relaxin / Q000627:therapeutic use*
D012065:Relaxin