Galectin-3 in Cardiac Remodeling and Heart Failure
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Galectin-3 is a member of the galectin family, which consists of animal lectins that bind β-galactosides. Recently, a role for galectin-3 in the pathophysiology of heart failure has been suggested. It was observed that galectin-3 is specifically upregulated in decompensated heart failure compared with compensated heart failure in animal models of heart failure. This has been associated with activation of fibroblasts and macrophages, which are a hallmark of cardiac remodeling. Therefore, galectin-3 may be a culprit biomarker in heart failure. Initial clinical observations indicate that galectin-3 may be a useful biomarker for decompensated heart failure, with incremental value over well-used “pressure-dependent” biomarkers, such as B-type natriuretic peptide. Future studies should focus on galectin-3 biology to better address the usefulness of galectin-3 as a biomarker and probe the usefulness of anti-galectin-3 therapy in treating heart failure.
KeywordsGalectin 3 Heart failure Prognosis Fibrosis Macrophages Biomarkers Renin-angiotensin system
This work was supported by the Netherlands Heart Foundation (grant 2007T046 to Dr. de Boer) and the Innovational Research Incentives Scheme program of the Netherlands Organization for Scientific Research (NWO VENI, grant 016.106.117, also to Dr. de Boer).
No potential conflicts of interest relevant to this article were reported.
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- 11.Rosenberg I, Cherayil BJ, Isselbacher KJ, Pillai S: Mac-2-binding glycoproteins. Putative ligands for a cytosolic β-galactoside lectin. J Biol Chem 1991, 266:18731–18736.Google Scholar
- 17.Hughes RC: The galectin family of mammalian carbohydrate-binding molecules. Biochem Soc Transact 1997, 25:1194–1198.Google Scholar
- 25.Sharma U, Rhaleb NE, Pokharel S, et al.: Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage. Am J Physiol 2008, 294:H1226–H1232.Google Scholar
- 26.• Liu YH, D’Ambrosio M, Liao TD, et al.: N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin. Am J Physiol Heart Circ Physiol 2009, 296:H404–H412. This article evaluates anti-galectin-3 therapy and demonstrates how it may reverse adverse cardiac remodeling, providing support for the hypothesis that anti-galectin therapy may be feasible.PubMedCrossRefGoogle Scholar
- 35.• Henderson NC, Mackinnon AC, Farnworth SL, et al.: Galectin-3 expression and secretion links macrophages to the promotion of renal fibrosis. Am J Pathol 2008, 172:288–298. This experimental study underscores the pivotal role of galectin-3 in the fibrosis process. Employing galectin-3 deficient mice, the authors show that galectin-3 regulates renal fibrosis.PubMedCrossRefGoogle Scholar
- 46.• de Boer RA, Voors AA, Muntendam P, et al.: Galectin-3: a novel mediator of heart failure development and progression. Eur J Heart Fail 2009, 11:811–817. This article provides a complete overview of the potential role of galectin-3 in the pathophysiology of heart failure.PubMedCrossRefGoogle Scholar
- 47.Dickstein K, Cohen-Solal A, Filippatos G, et al.: ESC guidelines for the diagnosis treatment of acute, chronic heart failure 2008. The task force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail 2008, 10:933–989.PubMedCrossRefGoogle Scholar