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Galectin-3 binding protein, coronary artery disease and cardiovascular mortality: Insights from the LURIC study
Christian A Gleissner1, Christian Erbel1, Fabian Linden2
1Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Heidelberg, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg, Germany.
Insights
Galectin-3 binding protein (Gal-3BP) levels are linked to increased mortality in coronary artery disease (CAD) patients. While not directly causal, Gal-3BP may contribute to cardiovascular risk through inflammation.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Immunology
Background:
- Galectin-3 binding protein (Gal-3BP) is implicated in inflammation and cancer.
- Its specific role in coronary artery disease (CAD) and cardiovascular outcomes is not well understood.
Purpose of the Study:
- To investigate the association between Gal-3BP plasma levels and cardiovascular outcomes in a large patient cohort.
- To explore potential causal links and underlying mechanisms of Gal-3BP in CAD.
Main Methods:
- Plasma Gal-3BP levels were measured in 2922 LURIC study participants using ELISA.
- Mortality data were analyzed using Kaplan-Meier and Cox regression.
- Mendelian randomization was employed to assess causality.
- In vitro studies examined Gal-3BP effects on macrophages.
Main Results:
- Higher Gal-3BP levels correlated with increased all-cause and cardiovascular mortality.
- Gal-3BP was independently associated with metabolic and inflammatory markers.
- In vitro, Gal-3BP induced a pro-inflammatory response in macrophages.
- Adding Gal-3BP improved risk assessment for patients with ESC SCORE >5%.
Conclusions:
- Gal-3BP levels are independently associated with mortality in CAD patients.
- Mechanisms likely involve metabolic and inflammatory distress.
- Further prospective studies are needed to confirm clinical utility.
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.