• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell metabolism >Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress.
【24h】

Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress.

机译：致动脉性脂质和脂蛋白在经历内质网应激的巨噬细胞中触发CD36-TLR2依赖性细胞凋亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Macrophage apoptosis in advanced atheromata, a key process in plaque necrosis, involves the combination of ER stress with other proapoptotic stimuli. We show here that oxidized phospholipids, oxidized LDL, saturated fatty acids (SFAs), and lipoprotein(a) trigger apoptosis in ER-stressed macrophages through a mechanism requiring both CD36 and Toll-like receptor 2 (TLR2). In vivo, macrophage apoptosis was induced in SFA-fed, ER-stressed wild-type but not Cd36(/) or Tlr2(/) mice. For atherosclerosis, we combined TLR2 deficiency with that of TLR4, which can also promote apoptosis in ER-stressed macrophages. Advanced lesions of fat-fed Ldlr(/) mice transplanted with Tlr4(/)Tlr2(/) bone marrow were markedly protected from macrophage apoptosis and plaque necrosis compared with WT -->Ldlr(/) lesions. These findings provide insight into how atherogenic lipoproteins trigger macrophage apoptosis in the setting of ER stress and how TLR activation might promote macrophage apoptosis and plaque necrosis in advanced atherosclerosis.
机译：晚期粥样斑块中的巨噬细胞凋亡是斑块坏死的关键过程，它涉及内质网应激与其他促凋亡刺激的结合。我们在这里显示氧化的磷脂，氧化的LDL，饱和脂肪酸（SFA）和脂蛋白（a）通过同时需要CD36和Toll样受体2（TLR2）的机制触发内质网应激的巨噬细胞凋亡。在体内，在SFA喂养，内质网应激的野生型中诱导巨噬细胞凋亡，但在Cd36（/）或Tlr2（/）小鼠中却没有。对于动脉粥样硬化，我们将TLR2缺乏症与TLR4缺乏症相结合，这也可以促进内质网应激的巨噬细胞的凋亡。与WT-> Ldlr（/）病变相比，移植了Tlr4（/）Tlr2（/）骨髓的脂肪喂养Ldlr（/）小鼠的晚期病变明显免受巨噬细胞凋亡和斑块坏死的影响。这些发现为深入了解动脉粥样硬化性脂蛋白如何在内质网应激中触发巨噬细胞凋亡以及TLR活化如何促进晚期动脉粥样硬化中巨噬细胞凋亡和斑块坏死提供了见识。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号