Lambert Jessica M, Lopez Elizabeth F, Lindsey Merry L
Medical Student Research Stipend Program, UTHSCSA, TX 78229-3900, USA.
Int J Cardiol. 2008 Nov 12;130(2):147-58. doi: 10.1016/j.ijcard.2008.04.059. Epub 2008 Jul 25.
Following myocardial infarction (MI), circulating blood monocytes respond to chemotactic factors, migrate into the infarcted myocardium, and differentiate into macrophages. At the injury site, macrophages remove necrotic cardiac myocytes and apoptotic neutrophils; secrete cytokines, chemokines, and growth factors; and modulate phases of the angiogenic response. As such, the macrophage is a primary responder cell type that is involved in the regulation of post-MI wound healing at multiple levels. This review summarizes what is currently known about macrophage functions post-MI and borrows literature from other injury and inflammatory models to speculate on additional roles. Basic science and clinical avenues that remain to be explored are also discussed.
心肌梗死(MI)后,循环血液中的单核细胞对趋化因子作出反应,迁移至梗死心肌,并分化为巨噬细胞。在损伤部位,巨噬细胞清除坏死的心肌细胞和凋亡的中性粒细胞;分泌细胞因子、趋化因子和生长因子;并调节血管生成反应的各个阶段。因此,巨噬细胞是一种主要的反应细胞类型,在多个层面参与心肌梗死后伤口愈合的调节。本综述总结了目前已知的心肌梗死后巨噬细胞的功能,并借鉴其他损伤和炎症模型的文献推测其其他作用。还讨论了有待探索的基础科学和临床途径。