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Published on: July 14, 2021
Reversal of cardiac fibrosis and related dysfunction by relaxin
Xiao-Jun Du1, Qi Xu, Edna Lekgabe
1Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, University of Melbourne, Melbourne, Australia. xiaojun.du@bakeridi.edu.au
Abstract:
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.
Insights
Relaxin peptide effectively reverses cardiac fibrosis, a key factor in heart disease. Further research is needed to explore its functional benefits and therapeutic potential.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Regenerative Medicine
Background:
- Cardiac fibrosis is a hallmark of heart disease, contributing to heart failure and arrhythmias.
- There is a significant need for effective antifibrotic therapies.
- Previous studies indicated a cardiac fibrosis phenotype in relaxin-1-deficient mice.
Purpose of the Study:
- To investigate the antifibrotic effects of relaxin in rodent models of cardiac fibrosis.
- To explore the potential of relaxin as a therapeutic agent for heart disease.
Main Methods:
- Treatment with relaxin peptide or viral gene delivery of relaxin in rodent models.
- Induction of transmural myocardial infarction in mice.
- Assessment of cardiac fibrosis reversal and scar density.
Main Results:
- Relaxin treatment reversed cardiac fibrosis in various rodent models.
- Relaxin therapy inhibited scar density in mice with myocardial infarction.
- Functional benefits of relaxin therapy were limited or underexplored in prior studies.
Conclusions:
- Relaxin demonstrates significant potential to reverse cardiac fibrosis through distinct mechanisms.
- Further investigation is warranted to evaluate functional improvements and antiarrhythmic potential.
- Relaxin may hold promise for stem cell-based therapies and antiarrhythmic treatments.
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