Relaxin and the extracellular matrix: molecular mechanisms of action and implications for cardiovascular disease.
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.
McGuane
Jonathan T
JT
Department of Zoology and Howard Florey Institute, University of Melbourne, Royal Parade, Parkville, 3010 Australia. j.mcguane@hfi.unimelb.edu.au
Parry
Laura J
LJ
D000818:Animals; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000473:pathology*; D004719:Endomyocardial Fibrosis / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000502:physiology*; D006801:Humans; D012065:Relaxin / Q000502:physiology*
D012065:Relaxin