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Theranostics. 2018 Jan 1;8(3):593-609. doi: 10.7150/thno.22196. eCollection 2018.

Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update.

Author information

1
University Medical Center Groningen, University of Groningen, Department of Cardiology, PO Box 30.001, 9700 RB Groningen, the Netherlands.
2
Massachusetts General Hospital, Cardiovascular Research Center, Boston, MA, USA.
3
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.

Abstract

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.

KEYWORDS:

Galectin-3; carbohydrate binding domain; cardiovascular disease; cell-cell adhesion; extracellular matrix; fibrosis; heart failure; interaction; renal disease

PMID:
29344292
PMCID:
PMC5771079
DOI:
10.7150/thno.22196
[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

Conflict of Interest: Dr. de Boer is employed by the UMC Groningen, that received research funding and consultancy fees from AstraZeneca, Bristol-Myers Squibb, Trevena, Roche, Thermo Fisher and Novartis. Dr. de Boer received speaker honoraria from Novartis. Dr. de Boer is a scientific founder of, consultant to, and has stock options of G3 Pharmaceuticals, a company that aims to develop galectin-3 inhibitors. Dr. Ho is a receiver of research supplies (modified citrus pectin) from Econugenics.

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