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Updated: Feb 15, 2026

Porcine Model of Infrarenal Abdominal Aortic Aneurysm
Published on: November 21, 2019
Galectin-3 and the incidence of abdominal aortic aneurysm: the atherosclerosis risk in communities (ARIC) study
Oluwaseun E Fashanu1, Aaron R Folsom1, Abayomi Oyenuga1
1Division of Epidemiology & Community Health, School of Public Health, University of MinnesotaMinneapolis, Minnesota, USA.
Abstract:
Galectin-3, a β-galactosidase binding lectin, known to be involved in inflammatory processes may be associated with abdominal aortic aneurysm (AAA) incidence. We examined the prospective association between plasma galectin-3 and incident AAA in 9,704 participants of the Atherosclerosis Risk in Communities (ARIC) study cohort. We followed participants from 1996-1998 through 2011 (124,260 person-years) for incident AAA (n=325) defined by ICD codes from hospital records and death certificates. At baseline, participants had a mean (SD) age of 62.8 (5.7) years; 20.9% were blacks and 56.5% females. The median (25th-75th percentile) galectin-3 level was 14.2 (12.0-16.9) ng/mL. Galectin-3 was correlated positively with most cardiovascular risk factors and with several cardiac or inflammatory biomarkers (C-reactive protein, troponin-T, and NT-proBNP). Using Cox proportional hazards regression adjusted for demographic variables and measured AAA risk factors, the hazard ratios for AAA across galectin-3 quintiles were 1 (Referent), 1.54 (1.05-2.26), 1.58 (1.05-2.41), 1.76 (1.15-2.72), and 1.92 (1.22-3.01) (p for trend =0.01). Further adjustment for the cardiac and inflammatory biomarkers largely attenuated the association between galectin-3 and AAA [AAA hazard ratio for galectin-3 Quintile 5 vs. Quintile 1: 1.29 (0.81-2.05); p-trend across quintiles =0.44]. In conclusion, higher concentrations of plasma galectin-3 were associated with greater incidence of AAA though not independent of other cardiac and inflammatory biomarkers. This reinforces that galectin-3, a systemic biomarker reflecting inflammation and probably increased systemic vascular resistance, is elevated early in the pathogenesis of AAA.
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