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Verfasst von:Gleißner, Christian A. [VerfasserIn]   i
 Erbel, Christian [VerfasserIn]   i
 Linden, Fabian [VerfasserIn]   i
 Domschke, Gabriele [VerfasserIn]   i
 Akhavanpoor, Mohammadreza [VerfasserIn]   i
 Helmes, Christian Michael [VerfasserIn]   i
 Dösch, Andreas [VerfasserIn]   i
 Kleber, Marcus E. [VerfasserIn]   i
 Katus, Hugo [VerfasserIn]   i
 März, Winfried [VerfasserIn]   i
Titel:Galectin-3 binding protein, coronary artery disease and cardiovascular mortality
Titelzusatz:insights from the LURIC study
Verf.angabe:Christian A. Gleissner, Christian Erbel, Fabian Linden, Gabriele Domschke, Mohammadreza Akhavanpoor, Christian M. Helmes, Andreas O. Doesch, Marcus E. Kleber, Hugo A. Katus, Winfried Maerz
E-Jahr:2017
Jahr:23 March 2017
Umfang:9 S.
Fussnoten:Gesehen am 01.08.2018
Titel Quelle:Enthalten in: Atherosclerosis
Ort Quelle:Amsterdam [u.a.] : Elsevier Science, 1970
Jahr Quelle:2017
Band/Heft Quelle:260(2017), Seite 121-129
ISSN Quelle:1879-1484
Abstract:Background and aims Galectin-3 binding protein (Gal-3BP) has been associated with inflammation and cancer, however, its role in coronary artery disease (CAD) and cardiovascular outcome remains unclear. Methods Gal-3BP plasma levels were measured by ELISA in 2922 individuals from the LURIC study (62.7 ± 10.6 years, 62.7% male). All-cause and cardiovascular mortality was assessed by Kaplan-Meier analysis and Cox proportional hazards regression. Causal involvement of Gal-3BP was tested for by Mendelian randomization. Gal-3BP effects on human monocyte-derived macrophages were assessed in vitro. Results During 8.8 ± 3.0 years, 866 individuals died, 654 of cardiovascular causes. There was a significant increase in all-cause and cardiovascular mortality with increasing Gal-3BP quintiles. After thorough adjustment, all-cause mortality remained significantly increased in the fifth Gal-3BP quintile (HRQ5 1.292 (1.030-1.620), p = 0.027); cardiovascular mortality remained increased in Gal-3BP quintiles two to five (HRQ51.433 (1.061-1.935, p = 0.019). Gal-3BP levels were not associated with diagnosis and extent of coronary artery disease. In addition, Mendelian randomization did not show a direct causal relationship between Gal-3BP levels and mortality. Gal-3BP levels were, however, independently associated with markers of metabolic and inflammatory distress. In vitro, Gal-3BP induced a pro-inflammatory response in human monocyte-derived macrophages. Adding Gal-3BP levels to the ESC score improved risk assessment in patients with ESC SCORE-based risk >5% (p = 0.010). Conclusions In a large clinical cohort of CAD patients, Gal-3BP levels are independently associated with all-cause and cardiovascular mortality. The underlying mechanisms may likely involve metabolic and inflammatory distress. To further evaluate the potential clinical value of Gal-3BP, prospective studies are needed.
DOI:doi:10.1016/j.atherosclerosis.2017.03.031
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: http://dx.doi.org/10.1016/j.atherosclerosis.2017.03.031
 Volltext: http://www.sciencedirect.com/science/article/pii/S0021915017301338
 DOI: https://doi.org/10.1016/j.atherosclerosis.2017.03.031
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Atherosclerosis
 Biomarker
 Coronary artery disease
 Inflammation
K10plus-PPN:1577926838
Verknüpfungen:→ Zeitschrift

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