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Review |
Chrishan S. Samuel, PhD, Howard Florey Institute of Experimental Physiology & Medicine and Department of Biochemisty & Molecular Biology, The University of Melbourne, Victoria 3010, Australia
Reprint Requests: Chrishan S. Samuel, PhD, Howard Florey Institute, University of Melbourne, Parkville, Victoria 3010, Australia; Tel: 613-8344-5653; Fax: 613-9348-1707; E-mail: c.samuel{at}hfi.unimelb.edu.au
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.
Key Words: Collagen • Gene-knockout mice • Fibrosis • Relaxin
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