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Genetic determinants of circulating galectin-3 levels in patients with coronary artery disease
Yu-Huang Liao1, Ming-Sheng Teng2, Jyh-Ming J Juang3,4
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei city, Taiwan.
Insights
Genetic variations in the LGALS3 gene significantly influence galectin-3 levels in coronary artery disease (CAD) patients. While galectin-3 levels correlate with inflammation markers, LGALS3 genotypes do not directly associate with these markers.
Area of Science:
- Cardiovascular Genetics
- Immunology
- Molecular Biology
Background:
- Galectin-3 is a key regulator of inflammation.
- Coronary artery disease (CAD) involves complex inflammatory processes.
- Understanding genetic influences on galectin-3 in CAD is crucial.
Purpose of the Study:
- To investigate the association between LGALS3 gene polymorphisms, galectin-3 serum levels, and inflammatory markers in patients with CAD.
- To determine the genetic contribution to galectin-3 levels in CAD.
- To explore the relationship between galectin-3 levels and specific inflammatory markers.
Main Methods:
- Genotyping of LGALS3 single nucleotide polymorphisms (SNPs) including rs2274273, rs4644, and rs4652.
- Measurement of serum galectin-3 levels in 474 CAD patients.
- Analysis of correlations between galectin-3 levels and various inflammatory markers (e.g., leukocyte count, C-reactive protein, ICAM-1, MMP-9).
- Multivariate analysis to assess the impact of LGALS3 genotypes on galectin-3 level variation.
Main Results:
- Significant correlations were observed between galectin-3 levels and leukocyte count, C-reactive protein, soluble intercellular adhesion molecule-1, and matrix metalloproteinase 9 (p < .05).
- LGALS3 genotypes (rs2274273, rs4644, rs4652) and haplotypes (CAC, CCC, ACT) were strongly associated with galectin-3 levels (p < 1.05 × 10⁻²⁵).
- LGALS3 rs2274273 and rs4644 genotypes explained 20.8% of the variation in galectin-3 levels.
- No association was found between LGALS3 genotypes and other measured inflammatory marker levels.
Conclusions:
- Galectin-3 levels in CAD patients are strongly influenced by genetic factors related to the LGALS3 gene.
- Elevated galectin-3 levels, but not specific LGALS3 genotypes, are associated with increased inflammatory markers in CAD.
- Further research is warranted to clarify the role of galectin-3 in the pathogenesis of chronic inflammatory diseases.
Background:
Galectin-3 plays a crucial role in the regulation of inflammation. The aim of this study was to elucidate the association between LGALS3 genotypes, galectin-3 levels, and inflammatory marker levels in patients with coronary artery disease (CAD).
Results:
A total of 474 patients with CAD were enrolled. Significant correlations were discerned between galectin-3 levels and leukocyte counts, C-reactive protein, soluble intercellular adhesion molecule-1, and matrix metalloproteinase 9 levels (all p < .05). The LGALS3 rs2274273, rs4644, rs4652 genotypes, and haplotypes CAC, CCC, and ACT exhibited a significant association with galectin-3 levels (for genotypes, p = 1.05 × 10-25 , 3.54 × 10-25 , and 2.74 × 10-7 , respectively). Multivariate analysis showed LGALS3 rs2274273 and rs4644 genotypes contributing to 20.8% variation of galectin-3 levels. However, there was no association between LGALS3 genotypes and other inflammatory marker levels.
Conclusions:
Our data showed strong genetic determinants of galectin-3 levels in patients with CAD. The galectin-3 levels, but not LGALS3 genotypes, were associated with multiple inflammatory marker levels. Further study may be necessary to elucidate the molecular mechanism of galectin-3 in the pathogenesis of chronic inflammatory disorders.
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