Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S1462399405009944; 30 September 2005
Jonathan T. McGuane and Laura J. Parry (2005) Relaxin and the extracellular matrix: molecular mechanisms of action and implications for cardiovascular disease.
Expert Rev. Mol. Med. Vol. 7, Issue 21, DOI: 10.1017/S1462399405009944

Relaxin and the extracellular matrix: molecular mechanisms of action and implications for cardiovascular disease

Jonathan T. McGuane and Laura J. Parry

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Myocardial fibrosis is a common endpoint in a variety of cardiac pathologies. It results from excessive accumulation of collagen and other materials that together comprise the extracellular matrix (ECM). In the past decade, the peptide hormone relaxin has emerged as an important regulator of the ECM within several organs, including the heart, and has been suggested as a novel therapeutic agent for the treatment of fibrotic disorders. This review summarises research on the anti-fibrotic actions of relaxin, outlines the potential mechanisms by which relaxin regulates the ECM in cardiovascular tissues and examines the implications of this research for the management of heart disease. Some of the contradictions in the literature are also addressed in order to clarify the role of relaxin as an anti-fibrotic factor in vivo.

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Figure 1. A generalised scheme of cardiac fibrosis.
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Figure 2. A schematic representation of prorelaxin.
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Table 1. A comparison of the human relaxins.
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