• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

含NOD样受体吡啉结构域蛋白3炎性小体与心肌缺血再灌注损伤

[NOD-like receptor pyrin domain containing 3 inflammasome and myocardial ischemia-reperfusion injury].

作者信息

Dong Bo, Zhou Shenghua, Yu Siyang, Tang Liang

机构信息

Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha 410011, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2017 Jul 28;42(7):848-853. doi: 10.11817/j.issn.1672-7347.2017.07.018.

DOI:10.11817/j.issn.1672-7347.2017.07.018
PMID:28845012
Abstract

Myocardial ischemia-reperfusion injury (MI/RI) is an inflammatory cascade process involving the interaction of multiple factors. In recent years, more and more evidence suggests that NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, an important component of the innate immune system, is closely associated with the inflammatory damage of MI/RI. Furthermore, blockage of NLRP3 inflammasome or the release of its downstream pro-inflammatory cytokines may provide new therapeutic targets for this disorder.

摘要

心肌缺血再灌注损伤(MI/RI)是一个涉及多种因素相互作用的炎症级联反应过程。近年来,越来越多的证据表明,核苷酸结合寡聚化结构域样受体含pyrin结构域3(NLRP3)炎性小体作为固有免疫系统的重要组成部分,与MI/RI的炎症损伤密切相关。此外,阻断NLRP3炎性小体或其下游促炎细胞因子的释放可能为该疾病提供新的治疗靶点。

相似文献

1
[NOD-like receptor pyrin domain containing 3 inflammasome and myocardial ischemia-reperfusion injury].含NOD样受体吡啉结构域蛋白3炎性小体与心肌缺血再灌注损伤
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2017 Jul 28;42(7):848-853. doi: 10.11817/j.issn.1672-7347.2017.07.018.
2
The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury.NLRP3 炎性体在心肌成纤维细胞中上调,并介导心肌缺血再灌注损伤。
Cardiovasc Res. 2013 Jul 1;99(1):164-74. doi: 10.1093/cvr/cvt091. Epub 2013 Apr 10.
3
TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury.TXNIP作为心肌缺血/再灌注损伤的一种新机制,介导心脏微血管内皮细胞中NLRP3炎性小体的激活。
Basic Res Cardiol. 2014;109(5):415. doi: 10.1007/s00395-014-0415-z. Epub 2014 Jul 12.
4
shRNA interference of NLRP3 inflammasome alleviate ischemia reperfusion-induced myocardial damage through autophagy activation.NLRP3炎性小体的短发夹RNA干扰通过自噬激活减轻缺血再灌注诱导的心肌损伤。
Biochem Biophys Res Commun. 2017 Dec 16;494(3-4):728-735. doi: 10.1016/j.bbrc.2017.10.111. Epub 2017 Oct 22.
5
Regulation and Function of the Nucleotide Binding Domain Leucine-Rich Repeat-Containing Receptor, Pyrin Domain-Containing-3 Inflammasome in Lung Disease.含核苷酸结合结构域富含亮氨酸重复序列受体、含吡啉结构域的3炎性小体在肺部疾病中的调控与功能
Am J Respir Cell Mol Biol. 2016 Feb;54(2):151-60. doi: 10.1165/rcmb.2015-0231TR.
6
NLRP3 Inflammasome Activation-Mediated Pyroptosis Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats.NLRP3 炎性小体激活介导的细胞焦亡加重糖尿病大鼠心肌缺血/再灌注损伤。
Oxid Med Cell Longev. 2017;2017:9743280. doi: 10.1155/2017/9743280. Epub 2017 Sep 14.
7
Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial Ischemia/Reperfusion Injury by Activation of RISK and Mitochondrial Pathways.NLRP3炎性小体的药理学抑制通过激活RISK和线粒体途径减轻心肌缺血/再灌注损伤
Oxid Med Cell Longev. 2016;2016:5271251. doi: 10.1155/2016/5271251. Epub 2016 Dec 8.
8
Naoxintong attenuates Ischaemia/reperfusion Injury through inhibiting NLRP3 inflammasome activation.脑心通通过抑制NLRP3炎性小体激活减轻缺血/再灌注损伤。
J Cell Mol Med. 2017 Jan;21(1):4-12. doi: 10.1111/jcmm.12915. Epub 2016 Oct 26.
9
Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation.丙酮酸乙酯通过调控 ROS 相关 NLRP3 炎性小体激活对心肌缺血再灌注损伤的保护作用。
Oxid Med Cell Longev. 2019 Jan 9;2019:4264580. doi: 10.1155/2019/4264580. eCollection 2019.
10
Genetic Deletion or Pharmacological Inhibition of Soluble Epoxide Hydrolase Ameliorates Cardiac Ischemia/Reperfusion Injury by Attenuating NLRP3 Inflammasome Activation.基因敲除或可溶性环氧化物水解酶的药理学抑制通过减轻 NLRP3 炎性小体激活改善心肌缺血/再灌注损伤。
Int J Mol Sci. 2019 Jul 17;20(14):3502. doi: 10.3390/ijms20143502.