Macrophages, atherosclerosis and the potential of netrin-1 as a novel target for future therapeutic intervention.
作者信息
Moore Kathryn J, Fisher Edward A
出版信息
Future Cardiol. 2012 May;8(3):349-52. doi: 10.2217/fca.12.30.
Abstract
摘要
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Macrophages, atherosclerosis and the potential of netrin-1 as a novel target for future therapeutic intervention.巨噬细胞、动脉粥样硬化以及netrin-1作为未来治疗干预新靶点的潜力。
Future Cardiol. 2012 May;8(3):349-52. doi: 10.2217/fca.12.30.
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本文引用的文献
1
The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques.神经免疫导向分子 netrin-1 通过抑制斑块内巨噬细胞的迁移来促进动脉粥样硬化的形成。
Nat Immunol. 2012 Jan 8;13(2):136-43. doi: 10.1038/ni.2205.
2
Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides.在非人类灵长类动物中抑制 miR-33a/b 可提高血浆高密度脂蛋白胆固醇并降低极低密度脂蛋白甘油三酯。
Nature. 2011 Oct 19;478(7369):404-7. doi: 10.1038/nature10486.
3
Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis.在小鼠体内拮抗 miR-33 可促进胆固醇逆向转运并使动脉粥样硬化消退。
J Clin Invest. 2011 Jul;121(7):2921-31. doi: 10.1172/JCI57275. Epub 2011 Jun 6.
4
Macrophages in the pathogenesis of atherosclerosis.动脉粥样硬化发病机制中的巨噬细胞。
Cell. 2011 Apr 29;145(3):341-55. doi: 10.1016/j.cell.2011.04.005.
5
Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe-/- mice during disease regression.在动脉粥样硬化斑块消退期间，受抑制的单核细胞募集导致 Apoe-/- 小鼠的巨噬细胞从斑块中被清除。
J Clin Invest. 2011 May;121(5):2025-36. doi: 10.1172/JCI43802. Epub 2011 Apr 18.
6
Reversal of hyperlipidemia with a genetic switch favorably affects the content and inflammatory state of macrophages in atherosclerotic plaques.通过基因开关逆转高血脂可改善动脉粥样硬化斑块中巨噬细胞的含量和炎症状态。
Circulation. 2011 Mar 8;123(9):989-98. doi: 10.1161/CIRCULATIONAHA.110.984146. Epub 2011 Feb 21.
7
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals.NLRP3 炎性小体对于动脉粥样硬化的形成是必需的，并且可以被胆固醇晶体激活。
Nature. 2010 Apr 29;464(7293):1357-61. doi: 10.1038/nature08938.
8
Macrophage death and defective inflammation resolution in atherosclerosis.动脉粥样硬化中的巨噬细胞死亡和炎症消退缺陷。
Nat Rev Immunol. 2010 Jan;10(1):36-46. doi: 10.1038/nri2675. Epub 2009 Dec 4.
9
Hypoxia-inducible factor-dependent induction of netrin-1 dampens inflammation caused by hypoxia.缺氧诱导因子依赖性的网蛋白-1诱导可减轻缺氧引起的炎症。
Nat Immunol. 2009 Feb;10(2):195-202. doi: 10.1038/ni.1683. Epub 2009 Jan 4.
10
CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima.CD36可调节小鼠和人类巨噬细胞对氧化型低密度脂蛋白的迁移反应，并可能促使巨噬细胞滞留于动脉内膜。
J Clin Invest. 2009 Jan;119(1):136-45. doi: 10.1172/JCI35535. Epub 2008 Dec 8.
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