Another goal of this thesis was to further unravel galectin-3 biology. We show that galectin-3 levels increase upon severe hypertension or micro-albuminuria. In addition, renal function is an important determinant of the present galectin-3 level. Furthermore, blood group also determines galectin-3 level. Possibly, the biological activity of galectin-3 is regulated by glycosylation, the addition of sugar groups.
However, the most important feature of galectin-3 is to serve as a target for therapy. Pectins, which are complex sugars extracted from natural food sources, are able to inhibit galectin-3-mediated effects. Administration of pectins in an animal model attenuates cardiac fibrosis and preserves cardiac function. The concept of galectin-3 inhibition could be an interesting addition to the current heart failure treatment regimen.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2017|
Bakker, S. (Creator), Dotinga, A. (Creator), Vonk, J. (Creator), Smidt, N. (Creator), Scholtens, S. (Creator), Swertz, M. (Creator), Wijmenga, C. (Creator), Wolffenbuttel, B. (Creator), Stolk, R. (Creator), van Zon, S. (Creator), Rosmalen, J. (Creator), Postma, D. S. (Creator), Boer ,de, R. (Creator), Navis, G. (Creator), Slaets, J. (Creator), Ormel, H. (Creator), van Dijk, F. (Creator) & Bolmer, B. (Data Manager), Lifelines, 2006