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Review
. 2020 Dec 3;21(23):9232.
doi: 10.3390/ijms21239232.

Galectin-3 in Cardiovascular Diseases

Affiliations
Review

Galectin-3 in Cardiovascular Diseases

Valeria Blanda et al. Int J Mol Sci. .

Abstract

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.

Keywords: Galectin-3; atherosclerosis; biomarker; cardiovascular diseases; inflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Galectin-3 (Gal-3) chimeric structure characterized by a carbohydrate recognition domain and a non-lectin N-terminal domain that promotes oligomerization, allowing for the formation of pentamers.
Figure 2
Figure 2
Schematic representation of main roles of Gal-3 in several physiologic and pathogenetic mechanisms.

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