Genetic Variants in the Vicinity of <i><scp>LGALS</scp>‐3</i> Gene and <i><scp>LGALS</scp></i>‐3 <scp>mRNA</scp> Expression in Advanced Carotid Atherosclerosis: An Exploratory Study

Djordjevic, A.; Živković, Maja; Stanković, Aleksandra; Zivotic, Ivan; Končar, Igor; Davidović, Lazar; Alavantić, Dragan

doi:10.1002/jcla.21996

Cited by 14 publications

(11 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on these data, the authors proposed a molecular mechanism by which Gal-3 modulates not only inflammation, but also vascular osteogenesis, with its expression necessary to acquire a complete osteoblast-like phenotype by VSMCs. Another study highlighted that Gal-3 over-expression in VSMCs induced collagen type I increased synthesis [50], supporting its role as a remodelling factor of the vascular wall [51].…”

Section: Gal-3 In Inflammation and Atherosclerosismentioning

confidence: 92%

Galectin-3 in Cardiovascular Diseases

Blanda

Bracale

Taranto

et al. 2020

IJMS

112

View full text Add to dashboard Cite

Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis.

show abstract

Section: Gal-3 In Inflammation and Atherosclerosismentioning

confidence: 92%

Galectin-3 in Cardiovascular Diseases

Blanda

Bracale

Taranto

et al. 2020

IJMS

112

View full text Add to dashboard Cite

show abstract

“…Unlike our observations, a report by Zhang et al (41) showed that both SNPs rs2274273 and rs4644 gene variants of LGALS-3 were associated with cardiovascular diseases in the Chinese population. Djordjevic et al (42) found that SNP rs2274273 gene variant was associated with LGALS-3 mRNA levels of expression in atherosclerosis tissue of human carotid plaque. Also, Djordjevic et al (13) found that rs2274273 SNP was significantly associated with relative expression levels of LGALS-3 with left-ventricular maladaptive remodelling and HF occurring six months after MI.…”

Section: Discussionmentioning

confidence: 99%

“…Djordjevic et al [42] found that SNP rs2274273 gene variant was associated with LGALS-3 mRNA levels of expression in atherosclerosis tissue of human carotid plaque.…”

Section: Discussionmentioning

confidence: 99%

Associations of galectin-3 expression and LGALS-3 (rs4652) gene variant with coronary artery disease risk in diabetics

et al. 2021

View full text Add to dashboard Cite

Background Galectin‑3 protein that is encoded by lectin galactoside-binding soluble-3 (LGALS-3) gene serves as an important genetic factor in type 2 diabetes mellitus (T2DM) and its cardiovascular obstacles in various populations. We aimed to elicit the pro-inflammatory effect of galectin-3 as determined by interleukin-6 (IL-6) serum levels and to explore the relationship between galectin-3 (LGALS-3 rs4652) gene variation and its expression levels with coronary artery disease (CAD) risk among T2DM Egyptian patients. Methods: 112 lean subjects were compared to 100 T2DM without CAD and 84 T2DM with CAD. A tetra-primer amplification refractory mutation system polymerase chain reaction was used to test LGALS-3 (rs4652) and galectin-3 expression was tested with a quantitative real-time polymerase chain reaction. Serum IL-6 was measured using an enzyme-linked immunosorbent assay. Results: We found that the prevalence of LGALS-3 (rs4652) AC genotype and galectin-3 gene expression levels in T2DM with CAD were significantly higher than the additional 2 groups and were correlated positively to IL-6 circulating levels also, the C allele carriers (AC+CC) had significantly higher relative Galectin-3 expression levels compared to the A allele carriers (AA). Conclusion: We concluded that galectin-3 expression levels and LGALS-3 (rs4652) AC genotype were coronary artery disease risk factors in type two diabetics among an Egyptian sample.

show abstract

“…Gal-3 is involved in all processes active in atherosclerosis: cell adhesion, cell activation and chemoattraction, cell growth and differentiation [84]. An increase expression of Gal-3 mRNA in human carotid atherosclerotic plaque tissue may be affected by rare genetic variants of the haplotype block, previously associated with Gal-3 circulating levels [85,86]. Diverse cellular processes in atherosclerosis are affected by microRNAs (miRs) and their expression are often tissue and disease-specific [87,88].…”

Section: Role Of Ras In Atherosclerosis Progression and Acute Complicmentioning

confidence: 99%

Involvement of the Renin‐Angiotensin System in Atherosclerosis

Kolaković¹,

Živković²,

Stanković³

2017

Renin-Angiotensin System - Past, Present and Future

Self Cite

View full text Add to dashboard Cite

The renin-angiotensin system (RAS) is a well known for its role in the regulation of the blood pressure (BP). Angiotensin II (Ang II), the main mediator of the RAS, may act either, as a systemic molecule or a locally produced factor. Within the vessel wall it has significant proinflammatory role by inducing the oxidative stress, secretion of inflammatory cytokines and adhesion molecules. Ang II could trigger proliferation of vascular smooth muscle cells (VSMC) and its migration to the outer layer of the vessel wall. It could induce the release of matrix metalloproteinase (MMPs), from human VSMC and thus increase susceptibility to rupture of atherosclerotic lesions. Binding of Ang II to AT1R/AT2R could have opposing actions in vascular injury. The ACE2/Ang (1-7)/Mas axis of the RAS also opposes the unfavourable actions of ACE/Ang II/ATR1 axis. Inhibition of RAS could reduce inflammation-associated processes in vasculature, independently of lowering BP. RAS is significantly modulated by the genes coding for this system. Certain genetic variants (SNPs) in the RAS genes have been denoted as the functional ones and have been associated with hypertension, cardiovascular phenotypes and atherosclerosis. Also, the genetic components of the RAS interfere with the regulators of gene expression by microRNAs (miRs).

show abstract

Genetic Variants in the Vicinity of LGALS‐3 Gene and LGALS‐3 mRNA Expression in Advanced Carotid Atherosclerosis: An Exploratory Study

Cited by 14 publications

References 40 publications

Galectin-3 in Cardiovascular Diseases

Galectin-3 in Cardiovascular Diseases

Associations of galectin-3 expression and LGALS-3 (rs4652) gene variant with coronary artery disease risk in diabetics

Involvement of the Renin‐Angiotensin System in Atherosclerosis

Contact Info

Product

Resources

About