Functional variation in LGALS2 confers risk of myocardial infarction and regulates lymphotoxin-α secretion in vitro

摘要: Myocardial infarction (MI) has become one of the leading causes death in world. Its pathogenesis includes chronic formation plaque inside vessel wall coronary artery and acute rupture artery, implicating a number inflammation-mediating molecules, such as cytokine lymphotoxin-α (LTA)1. Functional variations LTA are associated with susceptibility to MI2. Here we show that protein binds galectin-2, member galactose-binding lectin family3. Our case–control association study Japanese population showed single nucleotide polymorphism LGALS2 encoding galectin-2 is significantly MI. This genetic substitution affects transcriptional level vitro, potentially altered secretion LTA, which would then affect degree inflammation; however, its relevance other populations remains be clarified. Smooth muscle cells macrophages human atherosclerotic lesions expressed both LTA. findings thus suggest link between cascade