Galectin-3 Predicts Long-Term Cardiovascular Death in High-Risk Patients With Coronary Artery Disease

Maiolino, Giuseppe; Rossitto, Giacomo; Pedon, Luigi; Cesari, Maurizio; Frigo, Anna Chiara; Azzolini, Michele; Plebani, Mario; Rossi, Gian Paolo

doi:10.1161/atvbaha.114.304964

Cited by 104 publications

(81 citation statements)

References 37 publications

(34 reference statements)

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“…This disease process, known as atherothrombosis, can lead to ACS or stroke [17][18][19]. The influence of Gal-3 on both atherosclerotic plaque formation and destabilization has been confirmed in several studies [20][21][22].…”

Section: Galectin-3 and Atherosclerosismentioning

confidence: 99%

Galectin-3 in acute coronary syndrome

Agnello

Bivona

Sasso

et al. 2017

Clinical Biochemistry

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Section: Galectin-3 and Atherosclerosismentioning

confidence: 99%

Galectin-3 in acute coronary syndrome

Agnello

Bivona

Sasso

et al. 2017

Clinical Biochemistry

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“…Studies have shown that increased Gal-3 serum concentrations are associated with increased 2-year risk of HF after acute coronary syndrome (2 ), increased cumulative 10-year incidence of HF in the Framingham Offspring Cohort (3 ), and decreased 18-month survival among HF patients (4 ). More recent studies have shown that Gal-3 is an independent predictor of cardiovascular mortality in patients with and without prior cardiovascular disease (5,6 ). Furthermore, a metaanalysis of 3 separate studies suggested that Gal-3 discharge values in the upper tertile (Ͼ18 g/L) were predictive of 30-day readmission in HF patients (7 ).…”

confidence: 99%

Short- and Long-term Biologic Variability of Galectin-3 and Other Cardiac Biomarkers in Patients with Stable Heart Failure and Healthy Adults

Schindler¹,

Szymanski²,

Hock³

et al. 2016

Clinical Chemistry

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BACKGROUND Galectin-3 (Gal-3) has been suggested as a prognostic biomarker in heart failure (HF) patients that may better reflect disease progression than traditional markers, including B-type natriuretic peptide (BNP) and cardiac troponins. To fully establish the utility of any biomarker in HF, its biologic variability must be characterized. METHODS To assess biologic variability, 59 patients were prospectively recruited, including 23 male and 16 female patients with stable HF and 10 male and 10 female healthy individuals. Gal-3, BNP, and high-sensitivity cardiac troponin I (hs-cTnI) were assayed at 5 time points within a 3-week period to assess short-term biologic variability. Long-term (3-month) biologic variability was assessed with samples collected at enrollment and after 4, 8, and 12 weeks. RESULTS Among healthy individuals, mean short-term biologic variability, expressed as intraindividual CV (CVI), was 4.5% for Gal-3, 29.0% for BNP, and 14.5% for hs-cTnI; long-term biologic variability was 5.5% for Gal-3, 34.7% for BNP, and 14.7% for hs-cTnI. In stable HF patients, mean short-term biologic variability was 7.1% for Gal-3, 22.5% for BNP, and 8.5% for hs-cTnI, and mean long-term biologic variability was 7.7% for Gal-3, 27.6% for BNP, and 9.6% for hs-cTnI. CONCLUSIONS The finding that Gal-3 has minimal intraindividual biological variability adds to its potential as a useful biomarker in HF patients.

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“…16 In addition, Gal-3 was recently reported to have a prognostic value in patients with coronary artery disease, possibly related to its role in plaque destabilization. 17 Several inhibitors of Gal-3 have been described, such as the modified citrus pectin (MCP; a complex water soluble indigestible polysaccharide riche in β-galactose) being able to block the lectin's activity. 18 We have recently demonstrated that Gal-3 mediates the vascular remodeling and the cardiac fibrosis induced by aldosterone.…”

mentioning

confidence: 99%

Galectin-3 Blockade Inhibits Cardiac Inflammation and Fibrosis in Experimental Hyperaldosteronism and Hypertension

et al. 2015

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Hypertensive cardiac remodeling is accompanied by molecular inflammation and fibrosis, 2 mechanisms that finally affect cardiac function. At cardiac level, aldosterone promotes inflammation and fibrosis, although the precise mechanisms are still unclear. Galectin-3 (Gal-3), a β-galactoside–binding lectin, is associated with inflammation and fibrosis in the cardiovascular system. We herein investigated whether Gal-3 inhibition could block aldosterone-induced cardiac inflammation and fibrosis and its potential role in cardiac damage associated with hypertension. Aldosterone-salt–treated rats presented hypertension, cardiac inflammation, and fibrosis that were prevented by the pharmacological inhibition of Gal-3 with modified citrus pectin. Cardiac inflammation and fibrosis presented in spontaneously hypertensive rats were prevented by modified citrus pectin treatment, whereas Gal-3 blockade did not modify blood pressure levels. In the absence of blood pressure modifications, Gal-3 knockout mice were resistant to aldosterone-induced cardiac inflammation. In human cardiac fibroblasts, aldosterone increased Gal-3 expression via its mineralocorticoid receptor. Gal-3 and aldosterone enhanced proinflammatory and profibrotic markers, as well as metalloproteinase activities in human cardiac fibroblasts, effects that were not observed in Gal-3–silenced cells treated with aldosterone. In experimental hyperaldosteronism, the increase in Gal-3 expression was associated with cardiac inflammation and fibrosis, alterations that were prevented by Gal-3 blockade independently of blood pressure levels. These data suggest that Gal-3 could be a new molecular mechanism linking cardiac inflammation and fibrosis in situations with high-aldosterone levels, such as hypertension.

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Galectin-3 Predicts Long-Term Cardiovascular Death in High-Risk Patients With Coronary Artery Disease

Cited by 104 publications

References 37 publications

Galectin-3 in acute coronary syndrome

Galectin-3 in acute coronary syndrome

Short- and Long-term Biologic Variability of Galectin-3 and Other Cardiac Biomarkers in Patients with Stable Heart Failure and Healthy Adults

Galectin-3 Blockade Inhibits Cardiac Inflammation and Fibrosis in Experimental Hyperaldosteronism and Hypertension

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