Publication

Galectin-3 in heart failure: From biomarker to target for therapy

van der Velde, A. R., 2017, [Groningen]: Rijksuniversiteit Groningen. 295 p.

Research output: ThesisThesis fully internal (DIV)Academic

APA

van der Velde, A. R. (2017). Galectin-3 in heart failure: From biomarker to target for therapy. [Groningen]: Rijksuniversiteit Groningen.

Author

van der Velde, Allart Rogier. / Galectin-3 in heart failure : From biomarker to target for therapy. [Groningen] : Rijksuniversiteit Groningen, 2017. 295 p.

Harvard

van der Velde, AR 2017, 'Galectin-3 in heart failure: From biomarker to target for therapy', Doctor of Philosophy, University of Groningen, [Groningen].

Standard

Galectin-3 in heart failure : From biomarker to target for therapy. / van der Velde, Allart Rogier.

[Groningen] : Rijksuniversiteit Groningen, 2017. 295 p.

Research output: ThesisThesis fully internal (DIV)Academic

Vancouver

van der Velde AR. Galectin-3 in heart failure: From biomarker to target for therapy. [Groningen]: Rijksuniversiteit Groningen, 2017. 295 p.


BibTeX

@phdthesis{a8dc89a817a849b39d14ae0714222882,
title = "Galectin-3 in heart failure: From biomarker to target for therapy",
abstract = "This thesis describes the role of galectin-3 in heart failure. Galectin-3 is a protein that is secreted in our body during inflammation and tissue damage. It becomes released into the blood stream and can be measured with a blood test. As a biomarker, galectin-3 can be used for risk stratification in patients with heart failure. In our studies, we show that repeated measurements provide incremental prognostic information. Furthermore, galectin-3 is a marker of subclinical disease: it can be used to identify subjects in the general population that will develop heart failure in the future. Galectin-3 is also involved in cardiac fibrosis and is released after myocardial infarction. Baseline galectin-3 measurements in patients with a myocardial infarction predict infarct size and cardiac function. 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.",
author = "{van der Velde}, {Allart Rogier}",
year = "2017",
language = "English",
isbn = "978-94-6169-998-5",
publisher = "Rijksuniversiteit Groningen",
school = "University of Groningen",

}

RIS

TY - THES

T1 - Galectin-3 in heart failure

T2 - From biomarker to target for therapy

AU - van der Velde, Allart Rogier

PY - 2017

Y1 - 2017

N2 - This thesis describes the role of galectin-3 in heart failure. Galectin-3 is a protein that is secreted in our body during inflammation and tissue damage. It becomes released into the blood stream and can be measured with a blood test. As a biomarker, galectin-3 can be used for risk stratification in patients with heart failure. In our studies, we show that repeated measurements provide incremental prognostic information. Furthermore, galectin-3 is a marker of subclinical disease: it can be used to identify subjects in the general population that will develop heart failure in the future. Galectin-3 is also involved in cardiac fibrosis and is released after myocardial infarction. Baseline galectin-3 measurements in patients with a myocardial infarction predict infarct size and cardiac function. 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.

AB - This thesis describes the role of galectin-3 in heart failure. Galectin-3 is a protein that is secreted in our body during inflammation and tissue damage. It becomes released into the blood stream and can be measured with a blood test. As a biomarker, galectin-3 can be used for risk stratification in patients with heart failure. In our studies, we show that repeated measurements provide incremental prognostic information. Furthermore, galectin-3 is a marker of subclinical disease: it can be used to identify subjects in the general population that will develop heart failure in the future. Galectin-3 is also involved in cardiac fibrosis and is released after myocardial infarction. Baseline galectin-3 measurements in patients with a myocardial infarction predict infarct size and cardiac function. 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.

M3 - Thesis fully internal (DIV)

SN - 978-94-6169-998-5

PB - Rijksuniversiteit Groningen

CY - [Groningen]

ER -

ID: 38571022