...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Circulation journal >C-reactive protein (CRP) is not a mere marker, but an active pathogenic substance.
【24h】

C-reactive protein (CRP) is not a mere marker, but an active pathogenic substance.

机译：C反应蛋白（CRP）不仅是标志物，还是活性病原体。

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

C-reactive protein (CRP) is a well-known inflammatory biomarker. The 5-subunit protein is produced mainly in the liver, stimulated by interleukin-6. CRP binds many ligands, such as oxidized low-density lipoprotein, phosphocholine residues of bacteria, damaged cell membranes and complement. The CRP receptor may be FcyR. Binding to FcyRI and FcyRIIa increases phagocytosis and the release of inflammatory cytokines; and to the inhibitory receptor, Fc/RUb, blocks activating signals (Figure). Epidemiological studies show the usefulness of CRP for indicating increased risk of cardiovascular events; atherothrombotic events increase with increased CRP level. The inflammatory process is considered a major contributor to vascular events, thus CRP may be both "marker" and "maker" of atherosclerosis leading to cardiovascular events. However, there are conflicting findings about the pathogenicity of CRP. The most robust evidence against CRP pathogenicity is that experimental data showing a proinflammatory nature of CRP may be caused by contamination of lipopolysaccharide or other proinflammatory substances in CRP. But others have demonstrated that the effect of atherogenicity is not contamination. Histologi-cally, CRP transgenic mice with null FcyRI or Rlla show attenuated atherosclerosis, whereas FcyRIIb null mice show accelerated atherosclerosis, strongly suggesting the pathogenicity of CRP.
机译：C反应蛋白（CRP）是众所周知的炎症生物标志物。 5-亚基蛋白主要在白介素6刺激下在肝脏中产生。 CRP结合许多配体，例如氧化的低密度脂蛋白，细菌的磷胆碱残基，受损的细胞膜和补体。 CRP受体可以是FcγR。与FcγRI和FcγRIIa的结合增加了吞噬作用和炎性细胞因子的释放。抑制受体Fc / RUb则阻断激活信号（图）。流行病学研究表明，CRP有助于表明心血管事件的风险增加。血栓形成事件随CRP水平升高而增加。炎症过程被认为是血管事件的主要诱因，因此CRP可能是导致心血管事件的动脉粥样硬化的“标志”和“制造者”。但是，关于CRP的致病性存在矛盾的发现。针对CRP致病性的最有力证据是，表明CRP具有促炎性的实验数据可能是由于CRP中脂多糖或其他促炎性物质的污染所致。但是其他人证明，动脉粥样硬化的影响不是污染。在组织学上，具有无效FcyRI或Rlla的CRP转基因小鼠表现出减缓的动脉粥样硬化，而具有FcyRIIb无效的小鼠表现出加速的动脉粥样硬化，强烈暗示了CRP的致病性。

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