Critical Role of Macrophage Death in Plaque Progression

巨噬细胞死亡在斑块进展中的关键作用

• 批准号: 6678752
• 负责人: Stephen MARK Schwartz
• 金额: $ 40.52万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-09-30 至 2007-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6678752
• 关键词: apolipoprotein E; apoptosis; atherosclerosis; atherosclerotic plaque; bone marrow transplantation; cell death; coagulation factor V; disease /disorder model; gene expression; gene targeting; genetically modified animals; genome; in situ hybridization; laboratory mouse; low density lipoprotein receptor; macrophage; microarray technology; model design /development; monocyte; morphometry; pathologic process; phenotype; terminal nick end labeling; tissue /cell culture; vascular endothelium

This is an application for support for an ongoing program devoted to final events in atherosclerosis, that is rupture of the atherosclerotic plaque. The hypothesis explored is that macrophage death plays a critical role in progression of the lesion. To test this hypothesis, we propose a combination of an in vitro assay designed to identify genes controlling macrophage death and an animal model already demonstrated to show spontaneous plaque rupture. Work done under this program has the potential to identify novel therapeutic approaches to dealing with the progression from existing atherosclerotic lesions to atherosclerotic lesions that become clinically significant.

这是一份支持正在进行的项目的申请，该项目致力于动脉粥样硬化的最终事件，即动脉粥样硬化斑块的破裂。所探索的假设是巨噬细胞死亡在病变的进展中起着关键作用。为了检验这一假设，我们提出了一种旨在识别控制巨噬细胞死亡的基因的体外测定和已经证明显示自发斑块破裂的动物模型的组合。该计划下完成的工作有可能确定新的治疗方法来处理从现有动脉粥样硬化病变到动脉粥样硬化病变的进展 变得具有临床意义。