[1]郭双 邢栋 吕勃.程序性坏死、细胞焦亡与心肌缺血再灌注损伤[J].心血管病学进展,2020,(12):1255-1259.[doi:10.16806/j.cnki.issn.1004-3934.2020.12.008]
 GUO Shuang,XING Dong,LYU Bo.NecroptosisPyroptosis and Myocardial Ischemia-reperfusion Injury[J].Advances in Cardiovascular Diseases,2020,(12):1255-1259.[doi:10.16806/j.cnki.issn.1004-3934.2020.12.008]
点击复制

程序性坏死、细胞焦亡与心肌缺血再灌注损伤()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年12期
页码:
1255-1259
栏目:
综述
出版日期:
2020-12-25

文章信息/Info

Title:
NecroptosisPyroptosis and Myocardial Ischemia-reperfusion Injury
作者:
郭双 邢栋 吕勃
 (哈尔滨医科大学附属第二医院心内科,黑龙江 哈尔滨 150081)
Author(s):
GUO Shuang XING Dong LYU Bo
(Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University,Harbin 150081,Heilongjiang,China)
关键词:
心肌缺血再灌注损伤程序性坏死细胞焦亡NOD样受体家族含吡啶结构域炎性体半胱天冬酶gasderminD
Keywords:
Myocardial ischemia-reperfusion injury Necroptosis Pyroptosis Nucleotide - mediated oligomerization domain(NOD)-like receptor family pyrin domain containing Inflammasomes Caspase gasderminD
DOI:
10.16806/j.cnki.issn.1004-3934.2020.12.008
摘要:
冠状动脉粥样硬化性心脏病是威胁人类健康的主要疾病之一,会引起急性心肌梗死。目前针对心肌梗死,最有效的治疗是溶栓或经皮冠脉介入术治疗,恢复缺血冠状动脉的血流,减少梗死面积。然而,在治疗的同时,会发生缺血再灌注损伤,心肌细胞死亡。细胞死亡的方式研究较多的主要有两种:细胞凋亡和细胞坏死。后者包括程序性坏死和细胞焦亡。两种死亡形式与细胞凋亡不同,两者在形态学上有相同点,但在发生和执行机制上有所不同。这两种死亡方式贯穿于心肌缺血再灌注损伤的发生过程中。现就有关心肌缺血再灌注损伤的病理生理,以及程序性坏死和细胞焦亡的发生执行分子机制做一综述,其中NOD样受体家族含吡啶结构域、半胱天冬酶和gasderminD关键靶点有望为缺血心肌保护提供新的治疗思路。
Abstract:
Coronary atherosclerotic heart disease is one of the main diseases that threatening human health and can cause acute myocardial infarction .At present,the most effective treatment for myocardial infarction is thrombolytic therapy,or percutaneous coronary intervention,to restore the blood flow of ischemic coronary arteries and reduce the ischemic area.However,at the same time ischemia-reperfusion injury and myocardial cell death occurs.There are two main ways of cell death: apoptosis and necrosis.The latter includes necroptosis and pyroptosis.This two forms of death are different from apoptosis ,they are similar in morphology,but different in mechanism of occurrence and execution.These two modes of death are involved in the process of myocardial ischemia-reperfusion.This paper reviews the pathophysiology of myocardial ischemia-reperfusion injury and the molecular mechanism of the necroptosis and apoptosis, Nucleotide - mediated oligomerization domain (NOD) - like receptor family pyrin domain containing, Caspase and gasderminD, these key targets are expected to provide a new therapeutic approach for the protection of ischemic myocardium.

参考文献/References:


[1]Yellon DM,Hausenloy DJ.Myocardial reperfusion injury[J].N Engl J Med,2007,357(11):1121-1135.

[2]Pagliaro P,Moro F,Tullio F,et al.Cardioprotective pathways during reperfusion: focus on redox signaling and other moda lities of cell signaling[J].Antioxid Redox Signal,2011,14(5):833-850.

[3]Hausenloy DJ,Yellon DM. Myocradial ischemia-Reperfusion injury:a neglected therapeutic target[J]. Clin Invest ,2013,123(1):92-100.
[4]Hausenloy DJ,Yellon DM. Ischaemic conditioning and reperfusion injury[J]. Nat Rev Cardiol ,2016,13(4):193-209.

[5]Galluzzi L,Vitale I,Aaronson SA,et al. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death ,2018[J].Cell Death Differ,2018,25(3):486-541.

[6]Tonnus W,Meyer C,Paliege A,et al.The pathological features of regulated necrosis[J]. J Pathol ,2019,247(5):697-707.

[7]Liang H,Liu Y.Gasdermins pore cell membrane to pyroptosis[J].Sci China Life Sci,2016,59(10):1090-1092.

[8]Shalini S,Dorstyn L,Dawar S,et al.Old,new and emerging functions of caspases[J].Cell Death Differ,2015,22(4) :526-539.

[9]Grootjans S,Vanden Berghe T.Initiation and execution mechanisms of necroptosis:an overview[J].Cell Death Differ,2017,24(7):1184-1195.

[10]Cookson BT, Brennan MA. Pro-inflammatory programmed cell death[J].Trends Microbiol,2001,9(3):113-114.

[11]Galluzzi L,Vitale I,Abrams JM,et al.Molecular definitions of cell death subroutines:recommendations of the nomenclature committee on cell death 2012[J].Cell Death Differ,2012,19(1):107-120.

[12]Toldo S,Abbate A. The NLRP3 inflammasome in acute myocardial infarction[J]. Nat Rev Cardiol,2018,15(4):203-214.

[13]Man SM,Karki R,Kanneganti TD.Moleular mechanisms and functions of pyroptosis,inflammatory caspases and inflammasomes in infectious diseases[J].Immunol Rev,2017,277(1):61-75.

[14]Shi J,Zhao Y,Wang K,et al .Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature,2015,526(7575):660-665.

[15]Gong W,Shi Y,Ren J.Research progresses of molecular mechanism of pyroptosis and its related Diseases[J]. Immunobiology,2020,225(2):151884.

[16] Broz P,Pelegrin P,Shao F. The gasdermin,a protein family executing cell death and inflammation[J]. Nat Rev Immunol,2020,20(3):143-157.

[17]Kesavardhana S,Mailreddi RKS,Kanneganti TD. Caspases in the cell death,inflammation,and gasdermin-induced pyroptosis[J]. Annu Rev Immunol,2020 ,38:567-595.

[18]Zhang T,Zhang Y,Cui M,et al. CaMKⅡ is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis[J]. Nat Med ,2016,22(2): 175-182.

[19]Jia C,Chen H,Zhang J,et al.Role of pyroptosis in cardiovascular diseases[J].Int Immunopharmacol,2019,67:311-318.

[20]Choi ME,Price DR,Ryter SW,et al.Necroptosis:a crucial pathogenic mediator of human disease [J].JCI Insight,2019,4(15):e128834.

[21]Chen J,Kos R,Garssen J,et al.Molecular insights into the mechanism of necroptosis:the necrosome as a potential therapeutic target[J].Cells,2019,8(12):1486.

[22]Dmitriev YV,Minasian SM,Demchenko EA,et al. Study of cardioprotective effects of necroptosis inhibitors on isolated rat heart subjected to global ischemia-reperfusion[J]. Bull Exp Biol Med,2013,155(2): 214-217.

[23] Luedde M,Lutz M,Carter N,et al. RIP3,a kinase promoting necroptotic cell death,mediates adverse remodelling after myocardial infarction[J]. Cardiovasc Res,2014,103(2):206-216.

[24]Cruz SA,Qin Z,Stewart AFR,et al.Dabrafenib,an inhibitor of RIP3 kinase-dependent necroptosis,reduces ischemic brain injury[J]. Neural Regen Res,2018,13(2):252-256.

[25]Moerke C,Bleibaum F,Kunzendorf U ,et al. Combined knockout of RIPK3 and MLKL reveals unexpected outcome in tissue injury and inflammation[J]. Front Cell Dev Biol,2019,7:19.

[26]Zhou W,Chen C,Chen Z,et al.NLRP3:a novel mediator in cardiovascular disease[J]. Immunol Res,2018 ,2018:5702103.

[27]Sandanger ?,Gao E,Ranheim T,et al.NLRP3 inflammasome activation during myocardial ischemia reperfusion is cardioprotective[J]. Biochem Biophysl Res Commun ,2016,494(4):1012-1020.
[28]Toldo S,Marchetti C,Mauro AG,et al. Inhibition of the NLRP3 inflammasome limits the inflammatory injury following myocardial ischemia reperfusion in the mouse[J].Int J Cardiol,2016,209:215-220.

[29]Deftereos S,Giannopoulos G,Angelidis C,et al.Anti-inflammatory treatment with colchicine in acute myocardial infarction: A pilot study[J]. Circulation,2015,132(15):1395-1403,

[30]Tardif JC,Kouz S,Waters DD,et al.Efficacy and safety of low-dose colchicine after myocardial infarction[J]. N Engl J Med,2019,381(26):2497-2505.

[31]Rauf A,Shah M,Yellon DM,et al.The Role of caspase-1 in ischemia/reperfusion injury of the myocardium[J]. J Cardiovasc Pharmacol,2019,74(3):194-200.

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

[33]Audia JP,Yang XM,Crockett ES,et al. Caspase-1 inhibition by VX-765 administered at reperfusion in P2Y12 receptor antagonist treated rats provides long-term reduction in myocardial infarct size and preservation of ventricular function[J]. Basic Res Cardiol,2018,113(5):32.

[34]Ridker PM,Everett BM,Thuren T,et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease[J]. N Engl J Med,2017,377(12):1119-1131.

[35]Abbate A,Kontos MC,Abouzaki NA,et al. Comparative safety of interleukin-1 blockade with anakinra in patients with ST-segment elevation acute myocardial infarction (from the VCU-ART and VCU-ART2 pilot studies)[J]. Am J Cardiol,2015,115(3):288-292.

[36]Rathkey JK,Zhao J,Liu Z,et al.Chemical disruption of the pyroptotic pore-forming protein gasdermin D inhibits inflammatory cell death and sepsis[J]. Sci Immunol,2018,3,eaat2738.

[37]Zhang D,Qian J,ZhangP,et al.Gasdermin D serves as a key executioner of pyroptosis in experimental cerebral ischemia and Reperfusion model both in vivo and in vitro[J].J Neurosci Res,2019,97(6):645-660.

相似文献/References:

[1]阎萌,田芳,综述,等.程序性坏死与动脉粥样硬化[J].心血管病学进展,2016,(2):139.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.011]
 YAN Meng,TIAN Fang,TIAN Ye.Necroptosis and Atherosclerosis[J].Advances in Cardiovascular Diseases,2016,(12):139.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.011]
[2]张馨月 涂荣会.Toll样受体与心肌缺血再灌注损伤及其保护作用研究进展[J].心血管病学进展,2020,(2):172.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.018]
 ZHANG Xinyue,TU Ronghui.Review Onprotective Effects of Toll-like Receptors on Myocardial Ischemia Reperfusion Injury[J].Advances in Cardiovascular Diseases,2020,(12):172.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.018]
[3]张明 王敬萍.Nur77和GRP78与糖尿病心肌缺血再灌注损伤的关系研究[J].心血管病学进展,2020,(6):571.[doi:10.16806/j.cnki.issn.1004-3934.2020.06.003]
 ZHANG Ming Wang Jingping.Relationship between Nur77 and GRP78 and Myocardial Ischemia-reperfusion Injury in Diabetic Patients[J].Advances in Cardiovascular Diseases,2020,(12):571.[doi:10.16806/j.cnki.issn.1004-3934.2020.06.003]
[4]韩敏 朱兵 余嘉清 马依彤.程序性细胞死亡与心肌缺血再灌注损伤[J].心血管病学进展,2020,(10):1069.[doi:10.16806/j.cnki.issn.1004-3934.2020.10.017]
 HAN MinZHU BingYU JiaqingMA Yitong.  Programmed Cell Death and Myocardial Ischemic Reperfusion Injury[J].Advances in Cardiovascular Diseases,2020,(12):1069.[doi:10.16806/j.cnki.issn.1004-3934.2020.10.017]
[5]彭石 马茜钰 张丹 张兆元 张锦.铁死亡在心肌缺血再灌注损伤中的作用及靶向治疗研究进展[J].心血管病学进展,2022,(4):357.[doi:10.16806/j.cnki.issn.1004-3934.2022.04.017]
 PENG Shi,MA Qianyu,ZHANG Dan,et al.Role and Targeted Treatment of Ferroptosis?n Myocardial Ischemia Reperfusion Injury[J].Advances in Cardiovascular Diseases,2022,(12):357.[doi:10.16806/j.cnki.issn.1004-3934.2022.04.017]
[6]叶宇恒 钱玲玲 王如兴 李库林.心肌缺血再灌注损伤中铁死亡的调控机制研究进展[J].心血管病学进展,2023,(5):416.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.008]
 YE Yuheng,QIAN Lingling,WANG Ruxing,et al.Regulatory Mechanisms of Ferroptosis in Myocardial Ischemia Reperfusion Injury[J].Advances in Cardiovascular Diseases,2023,(12):416.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.008]
[7]李秋 李蔚华.TRIM蛋白家族在心肌缺血再灌注损伤中的研究进展[J].心血管病学进展,2023,(8):743.[doi:10.16806/j.cnki.issn.1004-3934.2023.08.016]
 LI Qiu,LI Weihua.Research Progress of TRIM Family in Myocardial Ischemia Reperfusion Injury[J].Advances in Cardiovascular Diseases,2023,(12):743.[doi:10.16806/j.cnki.issn.1004-3934.2023.08.016]
[8]李俊霖 韩虎魁 程攀科 李刚 陶剑虹.Foxp3+调节性T细胞与心肌缺血再灌注损伤概述[J].心血管病学进展,2023,(9):832.[doi:10.16806/j.cnki.issn.1004-3934.2023.09.015]
 LI Junlin,HAN Hukui,CHENG Panke,et al.Overview of Foxp3+ Regulatory T Cells and Myocardial Ischemia R eperfusion Injury[J].Advances in Cardiovascular Diseases,2023,(12):832.[doi:10.16806/j.cnki.issn.1004-3934.2023.09.015]
[9]冉黔松 周厚荣.长链非编码RNA调节自噬在心肌缺血再灌注损伤中的研究进展[J].心血管病学进展,2024,(3):238.[doi:10.16806/j.cnki.issn.1004-3934.2024.03.011]
 RAN Qiansong ZHOU Hourong.Long Non-Coding RNA Regulating Autophagy in Myocardial Ischemia-Reperfusion Injury[J].Advances in Cardiovascular Diseases,2024,(12):238.[doi:10.16806/j.cnki.issn.1004-3934.2024.03.011]
[10]热伊莱·开赛尔 谢翔.琥珀酸在心肌缺血再灌注损伤中的研究进展[J].心血管病学进展,2024,(8):722.[doi:10.16806/j.cnki.issn.1004-3934.202.08.011]
 Reyilai·Kaisaier,XIE Xiang.Succinic Acid and Myocardial Ischemia-Reperfusion Injury[J].Advances in Cardiovascular Diseases,2024,(12):722.[doi:10.16806/j.cnki.issn.1004-3934.202.08.011]
[11]郭双 吕勃.细胞凋亡和程序性坏死在心肌缺血再灌注损伤中的作用研究[J].心血管病学进展,2022,(12):1148.[doi:10.16806/j.cnki.issn.1004-3934.2022.12.020]
 GUO Shuang L YU Bo.The Role of Apoptosis and Necroptosis in Myocardial Ischemia-Reperfusion Injury[J].Advances in Cardiovascular Diseases,2022,(12):1148.[doi:10.16806/j.cnki.issn.1004-3934.2022.12.020]

备注/Memo

备注/Memo:
基金项目:国家自然基金青年科学基金(81400296);中国博士后科学基金(2017M61139);黑龙江省留学归国人员科学基金(LC201434)资助课题
通信作者:吕勃,E-mail:2855928554@qq.com
收稿日期:2020-06-01
更新日期/Last Update: 2021-02-22