我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

细胞焦亡在心血管疾病中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第1期
页码:
88-091
栏目:
综述
出版日期:
2017-10-10

文章信息/Info

Title:
Role of pyroptosis in cardiovascular diseases
作者:
赵汝舟1; 蒋 帅1; 侯 征2; 余志斌1
（第四军医大学：1.航空航天生理学教研室，2.药理学教研室，陕西 西安710032）
Author(s):
ZHAO Ru-zhou1;  JIANG Shuai1;  HOU Zheng2;  YU Zhi-bin1
(1.Department of Aerospace Physiology, 2.Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
细胞焦亡; caspase-1; 动脉粥样硬化; 心肌缺血/再灌注损伤
Keywords:
pyroptosis;  caspase-1;  atherosclerosis;  myocardial ischemia-reperfusion injury
分类号:
R392；R378
DOI:
-
文献标识码:
A
摘要:
细胞焦亡是一种新发现的细胞程序性死亡方式，该过程包含多种细胞因子的激活与降解。首先，细胞内炎症小体被激活，进而诱导半胱天冬酶（caspase）-1的激活和促炎症因子IL-1 和IL-18前体的降解。之后，细胞膜裂解与细胞核DNA片段化可导致IL-1 和IL-18释放，最终诱发炎症反应。机体固有免疫细胞经模式识别受体，识别病原相关分子模式或损伤相关分子模式，诱发细胞焦亡而清除病原体或损伤组织细胞，形成保护机体的一道有效屏障。越来越多的研究表明，在动脉粥样硬化(AS)的病理过程中，细胞焦亡不仅参与动脉粥样斑块的形成，也是促进斑块发展，甚至是影响斑块稳定性的重要因素。在心肌缺血/再灌注损伤中，细胞焦亡亦是MI区与边界区炎症反应的重要调控因子，其可影响修复期MI面积、纤维化程度与心功能。因此，细胞焦亡可能成为临床防治AS，以及促进缺血/再灌注心肌修复的新靶点。
Abstract:
Pyroptosis is programmed cell death characterized by activation or degradation of a series of cytokines. Intracellular inflammasomes are first activated, which induces the activation of caspase-1 and degradation of proinflammatory cytokines interleukin (IL)-1β and IL-18. Subsequently, disruption of cell membranes with fragmentation of nuclear DNA leads to IL-1 and IL-18 release, which finally induces inflammatory reaction. The innate immune cells of the body identify pathogen associated molecular patterns or damage associated molecular patterns via recognition receptor and then remove pathogens or damaged tissue cells by inducing pyroptosis, forming an effective barrier to protect the organism. A growing number of studies related to atherosclerosis have demonstrated that pyroptosis is not only involved in formation of atheromatous plaque, but also is a crucial factor which promotes the development and stability of plaques. In myocardial ischemia-reperfusion injury, pyroptosis is also an important regulatory factor of the inflammatory response in the myocardial infarct and border zones, which can affect myocardial infarct size, fibrosis degree, and cardiac function in the repair period. In summary, pyroptosis may become a novel therapeutic target for atherosclerosis and myocardial ischemia-reperfusion injury.

参考文献/References

[1]Vanden BT,Linkermann A,Jouan-Lanhouet S,et al.Regulated necrosis: the expanding network of non-apoptotic cell death pathways[J].Nat Rev Mol Cell Biol,2014,15(2):135-147.

[2]Brennan MA,Cookson BT.Salmonella induces macrophage death by caspase-1-dependent necrosis[J].Mol Microbiol,2000,38(1):31-40.

[3]Deretic V.Autophagy as an innate immunity paradigm: expanding the scope and repertoire of pattern recognition receptors[J].Curr Opin Immunol,2012,24(1):21-31.

[4]Deretic V,Saitoh T,Akira S.Autophagy in infection, inflammation and immunity[J].Nat Rev Immunol,2013,13(10):722-737.

[5]Saitoh T,Fujita N,Jang MH,et al.Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1beta production[J].Nature,2008,456 (7219):264-268.

[6]Jones SA,Mills KH,Harris J.Autophagy and inflammatory diseases[J].Immunol Cell Biol,2013,91(3):250-258.

[7]Byrne BG,Dubuisson JF,Joshi AD,et al.Inflammasome components coordinate autophagy and pyroptosis as macrophage responses to infection[J].MBio,2013,4(1):e00620- e00612.

[8]Chang W,Lin J,Dong J,et al.Pyroptosis: an inflammatory cell death implicates in atherosclerosis[J].Med Hypotheses,2013,81(3):484-486.

[9]Moore KJ,Tabas I.Macrophages in the pathogenesis of atherosclerosis[J].Cell,2011,145(3):341-355.

[10]Kolodgie FD,Narula J,Burke AP,et al.Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death[J].Am J Pathol,2000,157(4):1259-1268.

[11]Sarai M,Hartung D,Petrov A,et al.Broad and specific caspase inhibitor-induced acute repression of apoptosis in atherosclerotic lesions evaluated by radiolabeled annexin A5 imaging[J].J Am Coll Cardiol,2007,50(24):2305-2312.

[12]Thind GS,Agrawal PR,Hirsh B,et al.Mechanisms of myocardial ischemia-reperfusion injury and the cytoprotective role of minocycline:scope and limitations[J].Future Cardiol,2015,11(1):61-76.

[13]Bell RM,Bфtker HE,Carr RD,et al.9th Hatter Biannual Meeting:position document on ischaemia/reperfusion injury,conditioning and the ten commandments of cardioprotection[J].Basic Res Cardiol,2016,111(4):41.

[14]Takahashi M.NLRP3 inflammasome as a novel player in myocardial infarction[J].Int Heart J,2014,55(2):101-105.

[15]Kawaguchi M,Takahashi M,Hata T,et al.Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury[J].Circulation,2011,123 (6):594-604.

[16]Marchant DJ,Boyd JH,Lin DC,et al.Inflammation in myocardial diseases[J].Circ Res,2012,110(1):126-144.

备注/Memo

备注/Memo:
收稿日期: 2016-09-25.基金项目：国家自然科学基金项目资助（81571844） 通讯作者：余志斌，教授，主要从事应用心血管生理学研究 Email：yuzhib@fmmu.edu.cn 作者简介：赵汝舟，助教，硕士 Email：18791986290@163.com
更新日期/Last Update: 1900-01-01