Galectin-3 Is a Potential Mediator for Atherosclerosis

J Immunol Res. 2020 Feb 14:2020:5284728. doi: 10.1155/2020/5284728. eCollection 2020.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / epidemiology
  • Atherosclerosis / etiology*
  • Atherosclerosis / metabolism*
  • Atherosclerosis / pathology
  • Biomarkers
  • Blood Proteins
  • Disease Models, Animal
  • Disease Susceptibility*
  • Endothelium / metabolism
  • Foam Cells / immunology
  • Foam Cells / metabolism
  • Foam Cells / pathology
  • Galectin 3 / chemistry
  • Galectin 3 / genetics
  • Galectin 3 / metabolism*
  • Galectins
  • Humans
  • Inflammation / etiology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Macrophages / immunology
  • Macrophages / metabolism
  • Macrophages / pathology
  • Mice
  • Oxidative Stress

Substances

  • Biomarkers
  • Blood Proteins
  • Galectin 3
  • Galectins
  • LGALS3 protein, human