Galectin-3 Is a Potential Mediator for Atherosclerosis

Abstract

Atherosclerosis is a multifactorial chronic inflammatory arterial disease forming the pathological basis of many cardiovascular diseases such as coronary heart disease, heart failure, and stroke. Numerous studies have implicated inflammation as a key player in the initiation and progression of atherosclerosis. Galectin-3 (Gal-3) is a 30 kDa β-galactose, highly conserved and widely distributed intracellularly and extracellularly. Gal-3 has been demonstrated in recent years to be a novel inflammatory factor participating in the process of intravascular inflammation, lipid endocytosis, macrophage activation, cellular proliferation, monocyte chemotaxis, and cell adhesion. This review focuses on the role of Gal-3 in atherosclerosis and the mechanism involved and several classical Gal-3 agonists and antagonists in the current studies.

Figure 1

Gal-3 and its effect on different types of cells related to atherosclerosis. Gal-3: galectin-3; ox-LDL: oxidized low-density lipoprotein; VSMC: vascular smooth muscle cells; CRD: C-terminal carbohydrate recognition domain.

Figure 2

Diagram depicting the mechanisms by which Gal-3 promotes formation of atherosclerosis. Gal-3: galectin-3; TNF-α: tumor necrosis factor-α; IL-6: interleukin-6; CXCL8: C-X-C motif chemokine 8; CCL2: C-C chemokine ligand 2; CCL3: C-C chemokine ligand 3; CCL5: C-C chemokine ligand 5; ox-LDL: oxidized low-density lipoprotein; VSMC: vascular smooth muscle cells; AGEs: advanced glycation end products; NADPH II: nicotinamide-adenine dinucleotide phosphate II.