Galectin-3: A modifiable risk factor in heart failure

Rudolf A. De Boer, A. Rogier Van Der Velde, Christian Mueller, Dirk J. Van Veldhuisen, Stefan D. Anker, W. Frank Peacock, Kirkwood F. Adams, Alan Maisel

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)237-246
Number of pages10
JournalCardiovascular Drugs and Therapy
Issue number3
Publication statusPublished - 2014


  • Biomarker
  • Cardiac remodeling
  • Fibrosis
  • Galectin-3
  • Heart failure

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Cardiology and Cardiovascular Medicine
  • Pharmacology
  • Medicine(all)


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