Galectin-3 activation and inhibition in heart failure and cardiovascular disease: An update

Navin Suthahar, Wouter C. Meijers, Herman H.W. Silljé, Jennifer E. Ho, Fu-Tong Liu, Rudolf A. de Boer

Research output: Contribution to journalReview articlepeer-review

91 Scopus citations


Galectin-3 is a versatile protein orchestrating several physiological and pathophysiological processes in the human body. In the last decade, considerable interest in galectin-3 has emerged because of its potential role as a biotarget. Galectin-3 is differentially expressed depending on the tissue type, however its expression can be induced under conditions of tissue injury or stress. Galectin-3 overexpression and secretion is associated with several diseases and is extensively studied in the context of fibrosis, heart failure, atherosclerosis and diabetes mellitus. Monomeric (extracellular) galectin-3 usually undergoes further "activation" which significantly broadens the spectrum of biological activity mainly by modifying its carbohydrate-binding properties. Self-interactions of this protein appear to play a crucial role in regulating the extracellular activities of this protein, however there is limited and controversial data on the mechanisms involved. We therefore summarize (recent) literature in this area and describe galectin-3 from a binding perspective providing novel insights into mechanisms by which galectin-3 is known to be "activated" and how such activation may be regulated in pathophysiological scenarios.

Original languageEnglish (US)
Pages (from-to)593-609
Number of pages17
Issue number3
StatePublished - Jan 1 2018
Externally publishedYes


  • Carbohydrate binding domain
  • Cardiovascular disease
  • Cell-cell adhesion
  • Extracellular matrix
  • Fibrosis
  • Galectin-3
  • Heart failure
  • Interaction
  • Renal disease

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Pharmacology, Toxicology and Pharmaceutics (miscellaneous)


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