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Relaxin: antifibrotic properties and effects in models of disease
1Howard Florey Institute, University of Melbourne, Parkville, Victoria, Australia. c.samuel@hfi.unimelb.edu.au
Abstract:
Fibrosis (progressive scarring) is a leading cause of organ failure worldwide and causes loss of organ function when normal tissue is replaced with excess connective tissue. Several organs are prone to this process regardless of etiology. The pleiotropic hormone, relaxin, is emerging as a novel antifibrotic therapy. Relaxin has been shown to limit collagen production and reorganization, while stimulating increased collagen degradation. It not only prevents fibrogenesis, but also reduces established scarring. This review summarizes (1) the levels at which relaxin inhibits collagen production and existing collagen overexpression in induced models of fibrosis, and (2) the collagen-related phenotypes of relaxin- and LGR7-deficient mice. Recent studies on relaxin-deficient mice have established relaxin as an important, naturally occurring regulator of collagen turnover and provide new insights into the therapeutic potential of relaxin.
Insights
Relaxin, a hormone, shows promise as an antifibrotic therapy by limiting collagen production and enhancing its degradation. Studies in relaxin-deficient mice highlight its role in regulating collagen turnover for potential fibrosis treatment.
Area of Science:
- Biomedical Science
- Endocrinology
- Pathology
Background:
- Fibrosis, characterized by excessive connective tissue, is a major cause of organ failure globally.
- Current treatments for fibrosis are limited, necessitating novel therapeutic approaches.
- Relaxin, a pleiotropic hormone, is recognized for its potential antifibrotic properties.
Purpose of the Study:
- To review the mechanisms by which relaxin inhibits collagen production and degradation in fibrotic models.
- To examine the collagen-related phenotypes in mice lacking relaxin or its receptor (LGR7).
- To evaluate the therapeutic potential of relaxin in managing fibrosis.
Main Methods:
- Review of existing literature on relaxin's effects on collagen synthesis and degradation.
- Analysis of data from studies involving induced fibrosis models.
- Examination of genetic studies using relaxin- and LGR7-deficient mouse models.
Main Results:
- Relaxin effectively limits collagen production and reorganization while promoting collagen degradation.
- Studies demonstrate relaxin's ability to prevent fibrogenesis and reduce existing scar tissue.
- Relaxin-deficient mice exhibit altered collagen turnover, underscoring relaxin's regulatory role.
Conclusions:
- Relaxin emerges as a significant endogenous regulator of collagen turnover.
- Relaxin exhibits potent antifibrotic effects, offering therapeutic potential for various fibrotic conditions.
- Further research into relaxin-based therapies could lead to effective treatments for organ fibrosis.
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