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.
Highlights
Atherosclerosis has become the prelude and the major manifestation of ischemic coronary-cerebrovascular disease such as ischemic heart disease and stroke
Numerous studies have shown that Gal-3 contributes to macrophage differentiation, foam cell formation, endothelial dysfunction, and vascular smooth muscle cells (VSMC) proliferation and migration in atherosclerosis
We summarized several mechanisms pivotal to the development of atherosclerosis that are stimulated by local or circulating Gal-3
Summary
Atherosclerosis has become the prelude and the major manifestation of ischemic coronary-cerebrovascular disease such as ischemic heart disease and stroke. Atherosclerosis is a chronic inflammatory disease characterized by excessive accumulation of lipoprotein in macrophage, monocyte chemoattraction in vascular lesion, and the infiltration of vascular smooth muscle cells (VSMC) into the subendothelial space. Galectin-3 (Gal-3) is currently regarded as a potential cardiovascular inflammatory biomarker. It is a 29-35 kDa highly conserved β-galactoside-binding lectin and has received widespread interest in cardiovascular disease in recent decades. The role of Gal-3 in the cardiovascular area has been summarized by several review articles. Previous reviews mainly focused on the association between Gal-3 and heart failure [4,5,6], and the influence of Gal-3 on atherosclerosis has not been carefully summarized. This review summarizes the available research evidence on the effect of Gal-3 on atherosclerosis and the application of Gal-3 agonists and antagonists, with the aim of providing a better overview of Gal-3 as a new biomarker and contributor for atherosclerosis
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