LGALS3 and atherosclerosis: To elucidate the potential mechanisms underlying the accumulation of galectin-3–negative macrophages during plaque progression, we evaluated the effect of galectin-3 knockdown in human macrophages on the expression of genes commonly associated with macrophage motility, accumulation, and polarization,36 including MMPs proposed to play a role in atherosclerosis.6 Utilizing small interfering RNA, we observed on average a 77% knockdown of LGALS3 (lectin, galactoside-binding, soluble, 3; galectin-3) mRNA expression in primary human macrophages (Figure V in the Data Supplement).