离子通道调控急性心肌梗死中性粒细胞胞外诱捕网的研究进展

吴雨薇, 吴琼峰, 杜以梅. 离子通道调控急性心肌梗死中性粒细胞胞外诱捕网的研究进展[J]. 临床心血管病杂志, 2024, 40(5): 358-365. doi: 10.13201/j.issn.1001-1439.2024.05.003
引用本文: 吴雨薇, 吴琼峰, 杜以梅. 离子通道调控急性心肌梗死中性粒细胞胞外诱捕网的研究进展[J]. 临床心血管病杂志, 2024, 40(5): 358-365. doi: 10.13201/j.issn.1001-1439.2024.05.003
WU Yuwei, WU Qiongfeng, DU Yimei. Research progress of ion channels in the formation mechanism of neutrophil extracellular traps in acute myocardial infarction[J]. J Clin Cardiol, 2024, 40(5): 358-365. doi: 10.13201/j.issn.1001-1439.2024.05.003
Citation: WU Yuwei, WU Qiongfeng, DU Yimei. Research progress of ion channels in the formation mechanism of neutrophil extracellular traps in acute myocardial infarction[J]. J Clin Cardiol, 2024, 40(5): 358-365. doi: 10.13201/j.issn.1001-1439.2024.05.003

离子通道调控急性心肌梗死中性粒细胞胞外诱捕网的研究进展

  • 基金项目:
    国家自然科学基金项目(No:81900324、82170326)
详细信息

Research progress of ion channels in the formation mechanism of neutrophil extracellular traps in acute myocardial infarction

More Information
  • 中性粒细胞胞外诱捕网(neutrophil extracellular traps,NETs)是由组蛋白和中性粒细胞颗粒蛋白组成的DNA网状结构,在中性粒细胞捕获和杀死病原体过程中起重要作用。在心肌梗死过程中,中性粒细胞激活导致NETs水平的异常升高,加重了炎症反应和组织损伤。目前研究提示,相关离子通道的活化可通过不同途径调控NETs形成,导致心肌梗死后损伤加重、心律失常等心血管不良事件的发生。本文阐述了NETs的形成途径和对急性心肌梗死的作用,并详细描述了中性粒细胞上小电导钙激活钾通道、瞬时感受器电位离子通道、P2X受体和囊性纤维化跨膜电导调节体等在NETs形成中的作用和机制,为减轻心肌梗死后心脏重塑和心律失常提供新的思路。
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  • 图 1  离子通道参与NETs形成的作用和机制

    Figure 1.  The role and mechanism of ion channels on the formation of NETs

  • [1]

    Liew PX, Kubes P. The Neutrophil's Role During Health and Disease[J]. Physiol Rev, 2019, 99(2): 1223-1248. doi: 10.1152/physrev.00012.2018

    [2]

    Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria[J]. Science, 2004, 303(5663): 1532-1532. doi: 10.1126/science.1092385

    [3]

    Urban CF, Ermert D, Schmid M, et al. Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicans[J]. PLoS Pathog, 2009, 5(10): e1000639. doi: 10.1371/journal.ppat.1000639

    [4]

    Sorvillo N, Cherpokova D, Martinod K, et al. Extracellular DNA NET-Works With Dire Consequences for Health[J]. Circ Res, 2019, 125(4): 470-488. doi: 10.1161/CIRCRESAHA.119.314581

    [5]

    喻珮, 徐承义, 宋丹. 急性心肌梗死后心脏损伤修复的研究进展[J]. 临床心血管病杂志, 2023, 39(7): 558-562. https://www.cnki.com.cn/Article/CJFDTOTAL-LCXB202307013.htm

    [6]

    Eghbalzadeh K, Georgi L, Louis T, et al. Compromised Anti-inflammatory Action of Neutrophil Extracellular Traps in PAD4-Deficient Mice Contributes to Aggravated Acute Inflammation After Myocardial Infarction[J]. Front Immunol, 2019, 10: 2313. doi: 10.3389/fimmu.2019.02313

    [7]

    Immler R, Simon SI, Sperandio M. Calcium signalling and related ion channels in neutrophil recruitment and function[J]. Eur J Clin Invest, 2018, 48(Suppl 2): e12964.

    [8]

    Douda DN, Khan MA, Grasemann H, et al. SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx[J]. Proc Natl Acad Sci U S A, 2015, 112(9): 2817-2822. doi: 10.1073/pnas.1414055112

    [9]

    Ravindran M, Khan MA, Palaniyar N. Neutrophil Extracellular Trap Formation: Physiology, Pathology, and Pharmacology[J]. Biomolecules, 2019, 9(8): 365. doi: 10.3390/biom9080365

    [10]

    Thiam HR, Wong SL, Wagner DD, et al. Cellular Mechanisms of NETosis[J]. Annu Rev Cell Dev Biol, 2020, 36: 191-218. doi: 10.1146/annurev-cellbio-020520-111016

    [11]

    Skendros P, Mitroulis I, Ritis K. Autophagy in Neutrophils: From Granulopoiesis to Neutrophil Extracellular Traps[J]. Front Cell Dev Biol, 2018, 6: 109. doi: 10.3389/fcell.2018.00109

    [12]

    Helseth R, Shetelig C, Andersen GØ, et al. Neutrophil Extracellular Trap Components Associate with Infarct Size, Ventricular Function, and Clinical Outcome in STEMI[J]. Mediators Inflamm, 2019: 7816491.

    [13]

    Du M, Yang W, Schmull S, et al. Inhibition of peptidyl arginine deiminase-4 protects against myocardial infarction induced cardiac dysfunction[J]. Int Immunopharmacol, 2020, 78: 106055. doi: 10.1016/j.intimp.2019.106055

    [14]

    Vogel B, Shinagawa H, Hofmann U, et al. Acute DNase1 treatment improves left ventricular remodeling after myocardial infarction by disruption of free chromatin[J]. Basic Res Cardiol, 2015, 110(2): 15. doi: 10.1007/s00395-015-0472-y

    [15]

    Chen C, Zhang H, Xie R, et al. Gut microbiota aggravate cardiac ischemia-reperfusion injury via regulating the formation of neutrophils extracellular traps[J]. Life Sci, 2022, 303: 120670. doi: 10.1016/j.lfs.2022.120670

    [16]

    Abrams ST, Zhang N, Dart C, et al. Human CRP defends against the toxicity of circulating histones[J]. J Immunol, 2013, 191(5): 2495-2502. doi: 10.4049/jimmunol.1203181

    [17]

    Friggeri A, Banerjee S, Xie N, et al. Extracellular histones inhibit efferocytosis[J]. Mol Med, 2012, 18(1): 825-833.

    [18]

    Li YW, Chen SX, Yang Y, et al. Colchicine Inhibits NETs and Alleviates Cardiac Remodeling after Acute Myocardial Infarction[J]. Cardiovasc Drugs Ther, 2024, 38(1): 31-41. doi: 10.1007/s10557-022-07326-y

    [19]

    Chrysanthopoulou A, Mitroulis I, Apostolidou E, et al. Neutrophil extracellular traps promote differentiation and function of fibroblasts[J]. J Pathol, 2014, 233(3): 294-307. doi: 10.1002/path.4359

    [20]

    Hofbauer TM, Mangold A, Scherz T, et al. Neutrophil extracellular traps and fibrocytes in ST-segment elevation myocardial infarction[J]. Basic Res Cardiol, 2019, 114(5): 33. doi: 10.1007/s00395-019-0740-3

    [21]

    Zhang Z, Ding S, Wang Z, et al. Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis[J]. Acta Pharm Sin B, 2022, 12(4): 1840-1855. doi: 10.1016/j.apsb.2021.10.016

    [22]

    Mollenhauer M, Friedrichs K, Lange M, et al. Myeloperoxidase Mediates Postischemic Arrhythmogenic Ventricular Remodeling[J]. Circ Res, 2017, 121(1): 56-70. doi: 10.1161/CIRCRESAHA.117.310870

    [23]

    Rudolph V, Andrié RP, Rudolph TK, et al. Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation[J]. Nat Med, 2010, 16(4): 470-474. doi: 10.1038/nm.2124

    [24]

    Krause KH, Welsh MJ. Voltage-dependent and Ca2(+)-activated ion channels in human neutrophils[J]. J Clin Invest, 1990, 85(2): 491-498. doi: 10.1172/JCI114464

    [25]

    Fay AJ, Qian X, Jan YN, et al. SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes[J]. Proc Natl Acad Sci U S A, 2006, 103(46): 17548-17553. doi: 10.1073/pnas.0607914103

    [26]

    Mazzoleni V, Zimmermann K, Smirnova A, et al. Staphylococcus aureus Panton-Valentine Leukocidin triggers an alternative NETosis process targeting mitochondria[J]. FASEB J, 2021, 35(2): e21167.

    [27]

    Tackenberg H, Möller S, Filippi MD, et al. The Small GTPase Cdc42 Negatively Regulates the Formation of Neutrophil Extracellular Traps by Engaging Mitochondria[J]. Front Immunol, 2021, 12: 564720. doi: 10.3389/fimmu.2021.564720

    [28]

    Hundahl LA, Sattler SM, Skibsbye L, et al. Pharmacological blockade of small conductance Ca2+-activated K+ channels by ICA reduces arrhythmic load in rats with acute myocardial infarction[J]. Pflugers Arch, 2017, 469(5-6): 739-750. doi: 10.1007/s00424-017-1962-6

    [29]

    Takahashi M, Yokoshiki H, Mitsuyama H, et al. SK channel blockade prevents hypoxia-induced ventricular arrhythmias through inhibition of Ca2+/voltage uncoupling in hypertrophied hearts[J]. Am J Physiol Heart Circ Physiol, 2021, 320(4): H1456-H1469. doi: 10.1152/ajpheart.00777.2020

    [30]

    Najder K, Musset B, Lindemann O, et al. The function of TRP channels in neutrophil granulocytes[J]. Pflugers Arch, 2018, 470(7): 1017-1033. doi: 10.1007/s00424-018-2146-8

    [31]

    Massullo P, Sumoza-Toledo A, Bhagat H, et al. TRPM channels, calcium and redox sensors during innate immune responses[J]. Semin Cell Dev Biol, 2006, 17(6): 654-666. doi: 10.1016/j.semcdb.2006.11.006

    [32]

    Qian X, Zhao H, Chen X, et al. Disruption of transient receptor potential melastatin 2 decreases elastase release and bacterial clearance in neutrophils[J]. Innate Immun, 2018, 24(2): 122-130. doi: 10.1177/1753425918759181

    [33]

    Chauhan A, Sharma A, Tripathi JK, et al. Helminth derived factors inhibit neutrophil extracellular trap formation and inflammation in bacterial peritonitis[J]. Sci Rep, 2021, 11(1): 12718. doi: 10.1038/s41598-021-92001-9

    [34]

    Tripathi JK, Sharma A, Sukumaran P, et al. Oxidant sensor cation channel TRPM2 regulates neutrophil extracellular trap formation and protects against pneumoseptic bacterial infection[J]. FASEB J, 2018, 32(12): fj201800605.

    [35]

    Hiroi T, Wajima T, Negoro T, et al. Neutrophil TRPM2 channels are implicated in the exacerbation of myocardial ischaemia/reperfusion injury[J]. Cardiovasc Res, 2013, 97(2): 271-281. doi: 10.1093/cvr/cvs332

    [36]

    Nilius B, Szallasi A. Transient receptor potential channels as drug targets: from the science of basic research to the art of medicine[J]. Pharmacol Rev, 2014, 66(3): 676-814. doi: 10.1124/pr.113.008268

    [37]

    Parenti A, De Logu F, Geppetti P, et al. What is the evidence for the role of TRP channels in inflammatory and immune cells?[J]. Br J Pharmacol, 2016, 173(6): 953-969. doi: 10.1111/bph.13392

    [38]

    Yin J, Michalick L, Tang C, et al. Role of Transient Receptor Potential Vanilloid 4 in Neutrophil Activation and Acute Lung Injury[J]. Am J Respir Cell Mol Biol, 2016, 54(3): 370-383. doi: 10.1165/rcmb.2014-0225OC

    [39]

    卢凯. TRPV4调节中性粒细胞活化介导心肌缺血再灌注损伤机制的初步研究[D]. 华中科技大学, 2023.

    [40]

    王斌斌, 吴琼峰, 廖杰, 等. TRPV4通道与缺血再灌注损伤的研究进展[J]. 临床心血管病杂志, 2018, 34(7): 636-639. doi: 10.13294/j.aps.2015.0065

    [41]

    Wu QF, Qian C, Zhao N, et al. Activation of transient receptor potential vanilloid 4 involves in hypoxia/reoxygenation injury in cardiomyocytes[J]. Cell Death Dis, 2017, 8(5): e2828. doi: 10.1038/cddis.2017.227

    [42]

    Lecut C, Frederix K, Johnson DM, et al. P2X1 ion channels promote neutrophil chemotaxis through Rho kinase activation[J]. J Immunol, 2009, 183(4): 2801-2809. doi: 10.4049/jimmunol.0804007

    [43]

    Wang X, Chen D. Purinergic Regulation of Neutrophil Function[J]. Front Immunol, 2018, 9: 399. doi: 10.3389/fimmu.2018.00399

    [44]

    Wang X, Qin W, Xu X, et al. Endotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation[J]. Proc Natl Acad Sci U S A, 2017, 114(17): 4483-4488. doi: 10.1073/pnas.1616752114

    [45]

    Alarcón P, Manosalva C, Quiroga J, et al. Oleic and Linoleic Acids Induce the Release of Neutrophil Extracellular Traps via Pannexin 1-Dependent ATP Release and P2X1 Receptor Activation[J]. Front Vet Sci, 2020, 7: 260. doi: 10.3389/fvets.2020.00260

    [46]

    Quiroga J, Alarcón P, Manosalva C, et al. Mitochondria-derived ATP participates in the formation of neutrophil extracellular traps induced by platelet-activating factor through purinergic signaling in cows[J]. Dev Comp Immunol, 2020, 113: 103768. doi: 10.1016/j.dci.2020.103768

    [47]

    Lecut C, Faccinetto C, Delierneux C, et al. ATP-gated P2X1 ion channels protect against endotoxemia by dampening neutrophil activation[J]. J Thromb Haemost, 2012, 10(3): 453-465. doi: 10.1111/j.1538-7836.2011.04606.x

    [48]

    Zhuang S, Xia S, Huang P, et al. Targeting P2RX1 alleviates renal ischemia/reperfusion injury by preserving mitochondrial dynamics[J]. Pharmacol Res, 2021, 170: 105712. doi: 10.1016/j.phrs.2021.105712

    [49]

    Suh BC, Kim JS, Namgung U, et al. P2X7 nucleotide receptor mediation of membrane pore formation and superoxide generation in human promyelocytes and neutrophils[J]. J Immunol, 2001, 166(11): 6754-6763. doi: 10.4049/jimmunol.166.11.6754

    [50]

    Kim SW, Davaanyam D, Seol SI, et al. Adenosine Triphosphate Accumulated Following Cerebral Ischemia Induces Neutrophil Extracellular Trap Formation[J]. Int J Mol Sci, 2020, 21(20): 7668. doi: 10.3390/ijms21207668

    [51]

    Granado M, Amor S, Montoya JJ, et al. Altered expression of P2Y2 and P2X7 purinergic receptors in the isolated rat heart mediates ischemia-reperfusion injury[J]. Vascul Pharmacol, 2015, 73: 96-103. doi: 10.1016/j.vph.2015.06.003

    [52]

    Painter RG, Valentine VG, Lanson NA Jr, et al. CFTR Expression in human neutrophils and the phagolysosomal chlorination defect in cystic fibrosis[J]. Biochemistry, 2006, 45(34): 10260-10269. doi: 10.1021/bi060490t

    [53]

    Pohl K, Hayes E, Keenan J, et al. A neutrophil intrinsic impairment affecting Rab27a and degranulation in cystic fibrosis is corrected by CFTR potentiator therapy[J]. Blood, 2014, 124(7): 999-1009. doi: 10.1182/blood-2014-02-555268

    [54]

    Gray RD, Hardisty G, Regan KH, et al. Delayed neutrophil apoptosis enhances NET formation in cystic fibrosis[J]. Thorax, 2018, 73(2): 134-144. doi: 10.1136/thoraxjnl-2017-210134

    [55]

    Han H, Liu C, Li M, et al. Increased intracellular Cl-concentration mediates neutrophil extracellular traps formation in atherosclerotic cardiovascular diseases[J]. Acta Pharmacol Sin, 2022, 43(11): 2848-2861. doi: 10.1038/s41401-022-00911-9

    [56]

    Clauzure M, Valdivieso AG, Massip Copiz MM, et al. Disruption of interleukin-1β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator(CFTR)function[J]. PLoS One, 2014, 9(6): e99257. doi: 10.1371/journal.pone.0099257

    [57]

    Clauzure M, Valdivieso ÁG, Dugour AV, et al. NLR family pyrin domain containing 3(NLRP3) and caspase 1(CASP1) modulation by intracellular Cl-concentration[J]. Immunology, 2021, 163(4): 493-511. doi: 10.1111/imm.13336

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收稿日期:  2023-04-12
刊出日期:  2024-05-13

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