MACROPHAGE FATTY-ACID SYNTHASE DEFICIENCY DECREASES DIET-INDUCED ATHEROSCLEROSIS

巨噬细胞脂肪酸合酶缺乏可减少饮食引起的动脉粥样硬化

• 批准号: 8361454
• 负责人: Clay F. Semenkovich
• 金额: $ 0.43万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361454
• 关键词: Affect; Apolipoprotein E; Arterial Fatty Streak; Atherosclerosis; Diet; Fatty Acids; Fatty-acid synthase; Funding; Grant; Lesion; Mass Spectrum Analysis; Mus; National Center for Research Resources; Principal Investigator; Research; Research Infrastructure; Resources; Source; United States National Institutes of Health; biomedical resource; cost; fatty acid metabolism; macrophage

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Fatty acid metabolism is perturbed in atherosclerotic lesions, but whether it affects lesion formation is unknown. To determine whether fatty acid synthesis affects atherosclerosis, we inactivated fatty-acid synthase (FAS) in macrophages of apoE-deficient mice.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 脂肪酸代谢在动脉粥样硬化病变中受到干扰，但是它是否影响病变形成是未知的。为了确定脂肪酸合成是否影响动脉粥样硬化，我们在APOE缺陷小鼠的巨噬细胞中灭活脂肪酸合酶（FAS）。