Neutrophil Polarization Following Myocardial Infarction

摘要 大约四分之一的心肌梗塞（MI）患者发展为充血性心力衰竭， 五年死亡率为50%本项目的目标是了解MI后的角色， 中性粒细胞，通过建立这种细胞类型在伤口愈合过程中如何在表型中转变， 从炎症到修复我们假设中性粒细胞经历一个时间表型 包括影响MI后炎症消退和ECM组织。 具体目标1将绘制MI后时间过程中的中性粒细胞极化表型。目标2将 检验中性粒细胞积极促进炎症消退的假设。目标3将测试 中性粒细胞在瘢痕形成过程中积极参与细胞外基质组织化假说 阵创新在于评估MI后的中性粒细胞亚型，这将使我们能够 将早期中性粒细胞生理学与晚期重塑结果联系起来。多学科方法将 整合以探索中性粒细胞调节重塑的机制。本研究将 推动对LV重构细胞基础的理解，并确定新的干预措施 靶向中性粒细胞。

Abstract About one in four myocardial infarction (MI) patients progress to develop congestive heart failure, which has a 5-year mortality rate of 50%. The goal of this project is to understand post-MI roles of neutrophils by establishing how this cell type transitions in phenotype during wound healing spanning from inflammation to repair. We hypothesize that neutrophils undergo a temporal phenotype evolution that includes influencing post-MI inflammation resolution and ECM organization. Specific aim 1 will map neutrophil polarization phenotypes over the post-MI time course. Aim 2 will test the hypothesis that neutrophils actively contribute to inflammation resolution. Aim 3 will test the hypothesis that neutrophils actively contribute to extracellular matrix organization during scar formation. Innovation lies in the evaluation of neutrophil subtypes post-MI, which will allow us to connect early neutrophil cell physiology to late remodeling outcomes. Multi-discipline approaches will be integrated to explore the mechanisms whereby neutrophils regulate remodeling. This study will drive forward the understanding of the cellular basis of LV remodeling and identify novel intervention targets directed at neutrophils.