[1]焦亚琼 李育林 胡伯昂 钟明 韩露 宋铭.细胞焦亡在心肌缺血再灌注损伤中的作用[J].心血管病学进展,2024,(6):539.[doi:10.16806/j.cnki.issn.1004-3934.2024.06.014]
 JIAO Yaqiong,LI Yulin,HU Boang,et al.The Role of Pyroptosis in Myocardial Ischemia-Reperfusion Injury[J].Advances in Cardiovascular Diseases,2024,(6):539.[doi:10.16806/j.cnki.issn.1004-3934.2024.06.014]
点击复制

细胞焦亡在心肌缺血再灌注损伤中的作用()
分享到:

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

卷:
期数:
2024年6期
页码:
539
栏目:
综述
出版日期:
2024-06-25

文章信息/Info

Title:
The Role of Pyroptosis in Myocardial Ischemia-Reperfusion Injury
作者:
焦亚琼12 李育林13 胡伯昂1 钟明1 韩露12 宋铭1
(1.络病理论创新转化全国重点实验室 山东大学心血管重构与功能研究教育部 国家卫健委及中国医学科学院重点实验室 心血管转换医学省部共建国家重点实验室 山东大学齐鲁医院心血管内科,山东 济南 250012;2.山东大学齐鲁医院全科医学科,山东 济南 250012;3.山东第一医科大学附属省立医院心内科,山东 济南 250021)
Author(s):
JIAO Yaqiong12LI Yulin13HU Boang1ZHONG Ming1HAN Lu12SONG Ming1
(1.National Key Laboratory for Innovation and Transformation of Luobing Theory;The Key Laboratory of Cardiovascular Remodeling and Function Research,Chinese Ministry of Education,Chinese National Health Commission and Chinese Academy of Medical Sciences;Department of Cardiology,Qilu Hospital of Shandong University,Jinan 250012,Shandong,China;2.Department of General Practice,Qilu Hospital of Shandong University,Jinan 250012,Shandong,China;3.Department of Cardiology,Shandong Provincial Hospital Affiliated to Shandong First Medical University,Jinan 250001,Shandong,China)
关键词:
缺血再灌注损伤细胞焦亡氧化应激炎症反应药物治疗
Keywords:
Ischemia-Reperfusion InjuryPyroptosisOxidative StressInflammatory ResponseDrug therapy
DOI:
10.16806/j.cnki.issn.1004-3934.2024.06.014
摘要:
细胞焦亡是一种新型促炎性细胞程序性死亡方式,其由NOD样受体热蛋白结构域相关蛋白3(NLRP3)炎症小体活化启动,gasdermin D蛋白(gasdermin D,GSDMD)活性N端破坏细胞膜完整性,导致细胞死亡,随后引发炎症级联反应加重组织损伤。有研究表明,细胞焦亡可能参与心肌缺血再灌注损伤(MI/RI)的发生发展。MI/RI是限制急性心肌梗死临床疗效的重要原因之一。针对细胞焦亡的药物在MI/RI疾病模型中能够挽救焦亡所致心肌损伤。现就细胞焦亡在MI/RI中的作用做一综述,并在此基础上探讨可能的治疗靶点。
Abstract:
Pyroptosis is a novel pro-inflammatory programmed cell death modality,which is initiated by NOD-like receptor thermal protein domain associated protein 3(NLRP3) inflammasome activation ,and the active N-terminus of GSDMD destroys the integrity of the cell membrane,leading to cell death,and then triggering an inflammatory cascade to aggravate tissue damage. Studies have shown that pyroptosis may be involved in the development of myocardial ischemia-reperfusion injury (MI/RI). MIRI is one of the important reasons limiting the clinical efficacy of acute myocardial infarction. Drugs targeting pyroptosis can save myocardial injury caused by pyroptosis in a disease model of MI/RI. This article reviews the role of pyroptosis in myocardial ischemia-reperfusion injury,and discusses possible therapeutic targets on this basis

参考文献/References:

[1] Tsao CW,Aday AW,Almarzooq ZI,et al. Heart disease and stroke statistics-2023 update:a report from the American Heart Association[J]. Circulation,2023,147(8):e93-e621.

[2] Samsky MD,Morrow DA,Proudfoot AG,et al. Cardiogenic shock after acute myocardial infarction:a review[J]. JAMA,2021,326(18):1840-1850.

[3] Zhang H,Hu H,Zhai C,et al. Cardioprotective strategies after ischemia-reperfusion injury[J]. Am J Cardiovasc Drugs,2024,24(1):5-18.

[4] Algoet M,Janssens S,Himmelreich U,et al. Myocardial ischemia-reperfusion injury and the influence of inflammation[J]. Trends Cardiovasc Med,2023,33(6):357-366.

[5] Sun B,Wang L,Guo W,et al. New treatment methods for myocardial infarction[J]. Front Cardiovasc Med,2023,10:1251669.

[6] Chen M,Li X,Yang H,et al. Hype or hope:vagus nerve stimulation against acute myocardial ischemia-reperfusion injury[J]. Trends Cardiovasc Med,2020,30(8):481-488.

[7] Al Mamun A,Wu Y,Monalisa I,et al. Role of pyroptosis in spinal cord injury and its therapeutic implications[J]. J Adv Res,2020,28:97-109.

[8] Shi H,Gao Y,Dong Z,et al. GSDMD-mediated cardiomyocyte pyroptosis promotes myocardial I/R injury[J]. Circ Res,2021,129(3):383-396.

[9] Paik S,Kim JK,Silwal P,et al. An update on the regulatory mechanisms of NLRP3 inflammasome activation[J]. Cell Mol Immunol,2021,18(5):1141-1160.

[10] Lu LQ,Tian J,Luo XJ,et al. Targeting the pathways of regulated necrosis:a potential strategy for alleviation of cardio-cerebrovascular injury[J]. Cell Mol Life Sci,2021,78(1):63-78.

[11] Ji N,Qi Z,Wang Y,et al. Pyroptosis:a new regulating mechanism in cardiovascular disease[J]. J Inflamm Res,2021,14:2647-2666.

[12] Elias EE,Lyons B,Muruve DA. Gasdermins and pyroptosis in the kidney[J]. Nat Rev Nephrol,2023,19(5):337-350.

[13] Barnett KC,Li S,Liang K,et al. A 360°view of the inflammasome:mechanisms of activation, cell death, and diseases[J]. Cell,2023,186(11):2288-2312.

[14] Luan F,Rao Z,Peng L,et al. Cinnamic acid preserves against myocardial ischemia/reperfusion injury via suppression of NLRP3/Caspase-1/GSDMD signaling pathway[J]. Phytomedicine,2022,100:154047.

[15] Wu J,Cai W,Du R,et al. Sevoflurane Alleviates myocardial ischemia reperfusion injury by inhibiting P2X7-NLRP3 mediated pyroptosis[J]. Front Mol Biosci,2021,8:768594.

[16] Li H,Yang DH,Zhang Y,et al. Geniposide suppresses NLRP3 inflammasome-mediated pyroptosis via the AMPK signaling pathway to mitigate myocardial ischemia/reperfusion injury[J]. Chin Med,2022,17(1):73.

[17] Louwe MC,Olsen MB,Kaasb?ll OJ,et al. Absence of NLRP3 inflammasome in hematopoietic cells reduces adverse remodeling after experimental myocardial infarction[J]. JACC Basic Transl Sci,2020,5(12):1210-1224.

[18] Sun W,Lu H,Dong S,et al. Beclin1 controls caspase-4 inflammsome activation and pyroptosis in mouse myocardial reperfusion-induced microvascular injury[J]. Cell Commun Signal,2021,19(1):107.

[19] Li Q,Deng G,Gao Y. S100 calcium-binding protein A12 knockdown ameliorates hypoxia-reoxygenation-induced inflammation and apoptosis in human cardiomyocytes by regulating caspase-4-mediated non-classical pyroptosis[J]. Gen Physiol Biophys,2022,41(4):287-297.

[20] Qu Y,Gao R,Wei X,et al. Gasdermin D mediates endoplasmic reticulum stress via FAM134B to regulate cardiomyocyte autophagy and apoptosis in doxorubicin-induced cardiotoxicity[J]. Cell Death Dis,2022,13(10):901.

[21] Ye X,Hang Y,Lu Y,et al. CircRNA circ-NNT mediates myocardial ischemia/reperfusion injury through activating pyroptosis by sponging miR-33a-5p and regulating USP46 expression[J]. Cell Death Discov,2021,7(1):370.

[22] Han Y,Sun W,Ren D,et al. SIRT1 agonism modulates cardiac NLRP3 inflammasome through pyruvate dehydrogenase during ischemia and reperfusion[J]. Redox Biol,2020,34:101538.

[23] Jiang C,Wang Y,Guo M,et al. PCB118 induces inflammation of islet beta cells via activating ROS-NLRP3 inflammasome signaling[J]. Biomed Res Int,2021,2021:5522578.

[24] Cheng Y,Cheng L,Gao X,et al. Covalent modification of Keap1 at Cys77 and Cys434 by pubescenoside a suppresses oxidative stress-induced NLRP3 inflammasome activation in myocardial ischemia-reperfusion injury[J]. Theranostics,2021,11(2):861-877.

[25] Zhou Y,Li KS,Liu L,et al. MicroRNA-132 promotes oxidative stress?induced pyroptosis by?targeting sirtuin 1 in myocardial ischaemia-reperfusion injury[J]. Int J Mol Med,2020,45(6):1942-1950.

[26] Yu YW,Liu S,Zhou YY,et al. Shexiang Baoxin Pill attenuates myocardial ischemia/reperfusion injury by activating autophagy via modulating the ceRNA-Map3k8 pathway[J]. Phytomedicine,2022,104:154336.

[27] Huang KY,Liu S,Yu YW,et al. 3,4-benzopyrene aggravates myocardial ischemia-reperfusion injury-induced pyroptosis through inhibition of autophagy-dependent NLRP3 degradation[J]. Ecotoxicol Environ Saf,2023,254:114701.

[28] Jiang K,Xu Y,Wang D,et al. Cardioprotective mechanism of SGLT2 inhibitor against myocardial infarction is through reduction of autosis[J]. Protein Cell,2022,13(5):336-359.

[29] Mo G,Liu X,Zhong Y,et al. IP3R1 regulates Ca2+ transport and pyroptosis through the NLRP3/Caspase-1 pathway in myocardial ischemia/reperfusion injury[J]. Cell Death Discov,2021,7(1):31.

[30] Sun W,Lu H,Cui S,et al. NEDD4 ameliorates myocardial reperfusion injury by preventing macrophages pyroptosis[J]. Cell Commun Signal,2023,21(1):29.

[31] Wu Y,Zhang Y,Zhang J,et al. Cathelicidin aggravates myocardial ischemia/reperfusion injury via activating TLR4 signaling and P2X7R/NLRP3 inflammasome[J]. J Mol Cell Cardiol,2020,139:75-86.

[32] Zhang M,Lei YS,Meng XW,et al. Iguratimod alleviates myocardial ischemia/reperfusion injury through inhibiting inflammatory response induced by cardiac fibroblast pyroptosis via COX2/NLRP3 signaling pathway[J]. Front Cell Dev Biol,2021,9:746317.

[33] Ding HS,Huang Y,Qu JF,et al. Panaxynol ameliorates cardiac ischemia/reperfusion injury by suppressing NLRP3-induced pyroptosis and apoptosis via HMGB1/TLR4/NF-κB axis[J]. Int Immunopharmacol,2023,121:110222.

[34] Ye X,Zhang P,Zhang Y,et al. GSDMD contributes to myocardial reperfusion injury by regulating pyroptosis[J]. Front Immunol,2022,13:893914.

[35] Yanpiset P,Maneechote C,Sriwichaiin S,et al. Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury:cumulative evidence for future cardioprotective strategies[J]. Acta Pharm Sin B,2023,13(1):29-53.

[36] Mastrocola R,Penna C,Tullio F,et al. Pharmacological inhibition of NLRP3 inflammasome attenuates myocardial ischemia/reperfusion injury by activation of RISK and mitochondrial pathways[J]. Oxid Med Cell Longev,2016,2016:5271251.

[37] Chen X,Lin S,Dai S,et al. Trimetazidine affects pyroptosis by targeting GSDMD in myocardial ischemia/reperfusion injury[J]. Inflamm Res,2022,71(2):227-241.

[38] Audia JP,Yang XM,Crockett ES,et al. Caspase-1 inhibition by VX-765 administered at reperfusion in P2Y(12) 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.

[39] Zhong L,Han J,Fan X,et al. Novel GSDMD inhibitor GI-Y1 protects heart against pyroptosis and ischemia/reperfusion injury by blocking pyroptotic pore formation[J]. Basic Res Cardiol,2023,118(1):40.

[40] Liu N,Xie L,Xiao P,et al. Cardiac fibroblasts secrete exosome microRNA to suppress cardiomyocyte pyroptosis in myocardial ischemia/reperfusion injury[J]. Mol Cell Biochem,2022,477(4):1249-1260.

[41] Tang J,Jin L,Liu Y,et al. Exosomes derived from mesenchymal stem cells protect the myocardium against ischemia/reperfusion injury through inhibiting pyroptosis[J]. Drug Des Devel Ther,2020,14:3765-3775.

[42] Sandanger ?,Gao E,Ranheim T,et al. NLRP3 inflammasome activation during myocardial ischemia reperfusion is cardioprotective[J]. Biochem Biophys Res Commun,2016,469(4):1012-1020.

相似文献/References:

[1]陈丰 苏强 朱继金.高迁移率族蛋白B1在心脏炎症反应性疾病中的研究进展[J].心血管病学进展,2019,(8):1111.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.010]
 CHEN Feng,SU Qiang,ZHU Jijin.Research Progress of HMGB1 in Myocardial Inflammatory Reactivity Disease[J].Advances in Cardiovascular Diseases,2019,(6):1111.[doi:10.16806/j.cnki.issn.1004-3934.2019.08.010]
[2]王盛姣 关秀茹.MicroRNA与细胞焦亡在动脉粥样硬化中的作用研究[J].心血管病学进展,2020,(5):521.[doi:10.16806/j.cnki.issn.1004-3934.2020.05.019]
 WANG Shengjiao,GUAN Xiuru.MicroRNA and Pyroptosis in Atherosclerosis[J].Advances in Cardiovascular Diseases,2020,(6):521.[doi:10.16806/j.cnki.issn.1004-3934.2020.05.019]
[3]张依格 常盼 王西辉 王建榜.细胞焦亡在心血管疾病中的作用进展[J].心血管病学进展,2020,(7):724.[doi:10.16806/j.cnki.issn.1004-3934.2020.07.013]
 ZHANG Yige,CHANG Pan,WANG Xihui,et al.Role of Pyroptosis in Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2020,(6):724.[doi:10.16806/j.cnki.issn.1004-3934.2020.07.013]
[4]朱晓龙侯阳.细胞焦亡的分子机制其在心血管病变中的研究进展[J].心血管病学进展,2020,(8):847.[doi:10.16806/j.cnki.issn.1004-3934.2020.08.016]
 ZHU Xiaolong,HOU Yang.Molecular Mechanism of yroptosis and Its Research Progress in Cardiovascular Diseases[J].Advances in Cardiovascular Diseases,2020,(6):847.[doi:10.16806/j.cnki.issn.1004-3934.2020.08.016]
[5]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,(6):1069.[doi:10.16806/j.cnki.issn.1004-3934.2020.10.017]
[6]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.[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,(6):1255.[doi:10.16806/j.cnki.issn.1004-3934.2020.12.008]
[7]肖秋蓓 王志维.急性主动脉夹层并发急性肺损伤研究进展[J].心血管病学进展,2020,(12):1260.[doi:10.16806/j.cnki.issn.1004-3934.2020.12.009]
 XIAO QiubeiWANG Zhiwei.Acute Aortic Dissection Complicated with Acute Lung Injury[J].Advances in Cardiovascular Diseases,2020,(6):1260.[doi:10.16806/j.cnki.issn.1004-3934.2020.12.009]
[8]宋元秀 崔鸣.线粒体动力学异常与相关心血管疾病[J].心血管病学进展,2021,(2):162.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.017]
 SONG Yuanxiu,CUI Ming.Correlation Between Mitochondrial Dynamics and Cardiovascular Diseases[J].Advances in Cardiovascular Diseases,2021,(6):162.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.017]
[9]刘丽芳 彭瑜 张钲.急性ST段抬高型心肌梗死患者再灌注后心肌内出血的研究进展[J].心血管病学进展,2022,(5):444.[doi:10.16806/j.cnki.issn.1004-3934.2022.05.015]
 LIU Lifang,PENG Yu,ZHANG Zheng.Intracardial Hemorrhage After Reperfusion in Patients with Acute ST-Segment Elevation Myocardial Infarction[J].Advances in Cardiovascular Diseases,2022,(6):444.[doi:10.16806/j.cnki.issn.1004-3934.2022.05.015]
[10]王娟琳 黄颖.急性心肌梗死后心脏破裂机制的研究进展[J].心血管病学进展,2022,(7):619.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]
 WANG Juanlin,HUANG Ying.Mechanism of Cardiac Rupture After Acute Myocardial Infarction[J].Advances in Cardiovascular Diseases,2022,(6):619.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]

更新日期/Last Update: 2024-07-26