| Literature DB >> 24789662 |
Rudolf A de Boer1, A Rogier van der Velde, Christian Mueller, Dirk J van Veldhuisen, Stefan D Anker, W Frank Peacock, Kirkwood F Adams, Alan Maisel.
Abstract
Myocardial galectin-3 is upregulated upon cardiac stressors such as angiotensin II and pressure overload leading to cardiac remodeling and heart failure. The expression level of galectin-3 mirrors the progression and severity of heart failure and therefore, galectin-3 is being used as a biomarker for heart failure. However, as galectin-3 is causally involved in pathological myocardial fibrosis it has been suggested that galectin-3 also actively contributes to heart failure development. In this review we discuss how galectin-3 could be a target for therapy in heart failure. Currently, attempts are being made to target or inhibit galectin-3 using natural or pharmaceutical inhibitors with the aim to ameliorate heart failure. Available experimental evidence suggests that galectin-3 inhibition indeed may represent a novel tool to treat heart failure. A strong interaction with aldosterone, another strong pro-fibrotic factor, has been described. Clinical studies are needed to prove if galectin-3 may be used to install specific treatment regimens.Entities:
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Year: 2014 PMID： 24789662 DOI： 10.1007/s10557-014-6520-2
Source DB: PubMed Journal: Cardiovasc Drugs Ther ISSN： 0920-3206 Impact factor: 3.727