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Toll样受体在心肌梗死中的作用。

Role of toll-like receptors in myocardial infarction.

作者信息

Sun Yu, Liu Wen-Zhou, Liu Tao, Feng Xu, Yang Nuo, Zhou Hua-Fu

机构信息

a Department of Cardio-Thoracic Surgery , The First Affiliated Hospital of GuangXi Medical University , NanNing , China.

出版信息

J Recept Signal Transduct Res. 2015;35(5):420-2. doi: 10.3109/10799893.2014.993649. Epub 2014 Dec 17.

DOI:10.3109/10799893.2014.993649
PMID:25515816
Abstract

Toll-like receptors (TLRs) play a pivotal role in both innate and adaptive immunity, and TLRs recognize invading pathogens through molecular pattern recognition, and ultimately lead to the activation of transcription factors and inflammatory responses. Myocardial infarction leads to changes in the remodeling of the left ventricle of the heart, and the degree and type of remodeling provides important diagnostic information for the therapeutic management of ischemic heart disease. Innate immune takes a most important role in myocardial infarction. There are some studies reporting that TLRs play an important role in the myocardial infarction. The literatures were searched extensively and this review was performed to review the role of TLRs in myocardial infarction.

摘要

Toll样受体(TLRs)在固有免疫和适应性免疫中均发挥关键作用,TLRs通过分子模式识别来识别入侵的病原体,并最终导致转录因子的激活和炎症反应。心肌梗死会导致心脏左心室重构的改变,而重构的程度和类型为缺血性心脏病的治疗管理提供重要的诊断信息。固有免疫在心肌梗死中起着至关重要的作用。有一些研究报道TLRs在心肌梗死中发挥重要作用。我们广泛检索了文献,并进行了本综述以探讨TLRs在心肌梗死中的作用。

相似文献

1
Role of toll-like receptors in myocardial infarction.Toll样受体在心肌梗死中的作用。
J Recept Signal Transduct Res. 2015;35(5):420-2. doi: 10.3109/10799893.2014.993649. Epub 2014 Dec 17.
2
Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart.Toll样受体信号传导:心脏细胞存活和缺血性损伤的关键调节因子。
Am J Physiol Heart Circ Physiol. 2009 Jan;296(1):H1-12. doi: 10.1152/ajpheart.00995.2008. Epub 2008 Nov 14.
3
The innate immune response in reperfused myocardium.再灌注心肌中的固有免疫反应。
Cardiovasc Res. 2012 May 1;94(2):276-83. doi: 10.1093/cvr/cvs018. Epub 2012 Jan 20.
4
Toll like receptors and autoimmunity: a critical appraisal.Toll样受体与自身免疫:批判性评估
J Autoimmun. 2007 Dec;29(4):310-8. doi: 10.1016/j.jaut.2007.09.001. Epub 2007 Oct 24.
5
Toll-like receptors and innate immunity.Toll样受体与天然免疫
J Mol Med (Berl). 2006 Sep;84(9):712-25. doi: 10.1007/s00109-006-0084-y.
6
[Innate immunity: structure and function of TLRs].[固有免疫:Toll样受体的结构与功能]
Med Sci (Paris). 2007 Jan;23(1):67-73. doi: 10.1051/medsci/200723167.
7
Innate immunity: toll-like receptors and some more. A brief history, basic organization and relevance for the human newborn.固有免疫:Toll样受体及其他。简史、基本结构及其与人类新生儿的相关性。
Neonatology. 2007;92(3):145-57. doi: 10.1159/000102054. Epub 2007 Apr 27.
8
Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse.Toll样受体5缺陷加剧小鼠心肌缺血再灌注诱导的心脏损伤和炎症。
Clin Sci (Lond). 2015 Jul;129(2):187-98. doi: 10.1042/CS20140444.
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RAGE and TLRs: relatives, friends or neighbours?RAGE 和 TLRs:亲戚、朋友还是邻居?
Mol Immunol. 2013 Dec;56(4):739-44. doi: 10.1016/j.molimm.2013.07.008. Epub 2013 Aug 14.
10
Innate immune signaling in cardiac ischemia.心脏缺血中的先天免疫信号转导。
Nat Rev Cardiol. 2011 May;8(5):292-300. doi: 10.1038/nrcardio.2011.38. Epub 2011 Mar 29.

引用本文的文献

1
TLR4-A Pertinent Player in Radiation-Induced Heart Disease?TLR4 是否为放射性心脏病的相关靶点?
Genes (Basel). 2023 Apr 28;14(5):1002. doi: 10.3390/genes14051002.
2
Inhibition of MyD88 by a novel inhibitor reverses two-thirds of the infarct area in myocardial ischemia and reperfusion injury.一种新型抑制剂对髓样分化因子88(MyD88)的抑制作用可使心肌缺血再灌注损伤中的梗死面积缩小三分之二。
Am J Transl Res. 2020 Sep 15;12(9):5151-5169. eCollection 2020.
3
TLR9 is essential for HMGB1-mediated post-myocardial infarction tissue repair through affecting apoptosis, cardiac healing, and angiogenesis.
TLR9 通过影响细胞凋亡、心脏修复和血管生成对于心肌梗死后的组织修复是必不可少的。
Cell Death Dis. 2019 Jun 17;10(7):480. doi: 10.1038/s41419-019-1718-7.
4
Inflammation in myocardial injury: mesenchymal stem cells as potential immunomodulators.心肌损伤中的炎症:间充质干细胞作为潜在的免疫调节剂。
Am J Physiol Heart Circ Physiol. 2019 Aug 1;317(2):H213-H225. doi: 10.1152/ajpheart.00065.2019. Epub 2019 May 24.