Theranostics 2018; 8(3):593-609. doi:10.7150/thno.22196
Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update
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
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, fibrosis, extracellular matrix, heart failure, renal disease, cardiovascular disease, interaction, cell-cell adhesion, carbohydrate binding domain
Suthahar N, Meijers WC, Silljé HHW, Ho JE, Liu FT, de Boer RA. Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update. Theranostics 2018; 8(3):593-609. doi:10.7150/thno.22196. Available from http://www.thno.org/v08p0593.htm