留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

DAMP与NET在器官缺血-再灌注损伤中作用新进展

邹志锐 满江位 杨立

邹志锐, 满江位, 杨立. DAMP与NET在器官缺血-再灌注损伤中作用新进展[J]. 器官移植, 2021, 12(6): 761-766. doi: 10.3969/j.issn.1674-7445.2021.06.018
引用本文: 邹志锐, 满江位, 杨立. DAMP与NET在器官缺血-再灌注损伤中作用新进展[J]. 器官移植, 2021, 12(6): 761-766. doi: 10.3969/j.issn.1674-7445.2021.06.018
Zou Zhirui, Man Jiangwei, Yang Li. Recent progress on the roles of DAMP and NET in organ ischemia-reperfusion injury[J]. ORGAN TRANSPLANTATION, 2021, 12(6): 761-766. doi: 10.3969/j.issn.1674-7445.2021.06.018
Citation: Zou Zhirui, Man Jiangwei, Yang Li. Recent progress on the roles of DAMP and NET in organ ischemia-reperfusion injury[J]. ORGAN TRANSPLANTATION, 2021, 12(6): 761-766. doi: 10.3969/j.issn.1674-7445.2021.06.018

DAMP与NET在器官缺血-再灌注损伤中作用新进展

doi: 10.3969/j.issn.1674-7445.2021.06.018
基金项目: 

甘肃省自然科学基金 17JR5RA237

兰州大学第二医院“萃英科技创新”计划 CY2018-BJ02

详细信息
    作者简介:

    邹志锐,男,1996年生,硕士研究生,研究方向为肾脏缺血-再灌注损伤,Email: zouzhirui1996ts@163.com

    通讯作者:

    杨立,男,1971年生,博士,主任医师,研究方向为肾移植,Email: ery_yangli@lzu.edu.cn

  • 中图分类号: R617, R392.12

Recent progress on the roles of DAMP and NET in organ ischemia-reperfusion injury

More Information
  • 摘要: 缺血-再灌注损伤(IRI)是一种常见的病理生理现象,继发于器官移植、急性肾损伤、心肌梗死等众多病理过程中,显著增加了疾病严重程度与患者病死率。无菌性炎症是IRI的重要机制之一。细胞损伤相关分子模式(DAMP)是介导无菌性炎症的重要物质,其释放到胞外,通过与模式识别受体(PRR)结合,可有效激活免疫系统,启动并维持炎症反应。中性粒细胞胞外诱捕网(NET)是在炎症反应过程中由中性粒细胞释放的以DNA为骨架,含有组蛋白与众多颗粒蛋白的网状结构。近些年研究发现,DAMP与NET可通过无菌性炎症加剧IRI。本文回顾了DAMP、NET及其相互关系在IRI中的相关研究,对于理解IRI的病理生理学机制以及研究相应的防治策略有着重要的意义。

     

  • [1] LAND WG, AGOSTINIS P, GASSER S, et al. Transplantation and damage-associated molecular patterns (DAMPs)[J]. Am J Transplant, 2016, 16(12): 3338-3361. DOI: 10.1111/ajt.13963.
    [2] KALOGERIS T, BAINES CP, KRENZ M, et al. Ischemia/reperfusion[J]. Compr Physiol, 2016, 7(1): 113-170. DOI: 10.1002/cphy.c160006.
    [3] GONG T, LIU L, JIANG W, et al. DAMP-sensing receptors in sterile inflammation and inflammatory diseases[J]. Nat Rev Immunol, 2020, 20(2): 95-112. DOI: 10.1038/s41577-019-0215-7.
    [4] BRINKMANN V, REICHARD U, GOOSMANN C, et al. Neutrophil extracellular traps kill bacteria[J]. Science, 2004, 303(5663): 1532-1535. DOI: 10.1126/science.1092385.
    [5] BRAZA F, BROUARD S, CHADBAN S, et al. Role of TLRs and DAMPs in allograft inflammation and transplant outcomes[J]. Nat Rev Nephrol, 2016, 12(5): 281-290. DOI: 10.1038/nrneph.2016.41.
    [6] SILK E, ZHAO H, WENG H, et al. The role of extracellular histone in organ injury[J]. Cell Death Dis, 2017, 8(5): e2812. DOI: 10.1038/cddis.2017.52.
    [7] SHAH M, YELLON DM, DAVIDSON SM. The role of extracellular DNA and histones in ischaemia-reperfusion injury of the myocardium[J]. Cardiovasc Drugs Ther, 2020, 34(1): 123-131. DOI: 10.1007/s10557-020-06946-6.
    [8] HUANG H, TOHME S, AL-KHAFAJI AB, et al. Damage-associated molecular pattern-activated neutrophil extracellular trap exacerbates sterile inflammatory liver injury[J]. Hepatology, 2015, 62(2): 600-614. DOI: 10.1002/hep.27841.
    [9] LI T, JIANG H, LIU H, et al. Extracellular histones and xenotransplantation[J]. Xenotransplantation, 2020, 27(5): e12618. DOI: 10.1111/xen.12618.
    [10] NAKAZAWA D, KUMAR SV, MARSCHNER J, et al. Histones and neutrophil extracellular traps enhance tubular necrosis and remote organ injury in ischemic AKI[J]. J Am Soc Nephrol, 2017, 28(6): 1753-1768. DOI: 10.1681/ASN.2016080925.
    [11] ZHAO H, HUANG H, ALAM A, et al. VEGF mitigates histone-induced pyroptosis in the remote liver injury associated with renal allograft ischemia-reperfusion injury in rats[J]. Am J Transplant, 2018, 18(8): 1890-1903. DOI: 10.1111/ajt.14699.
    [12] LIEW FY, GIRARD JP, TURNQUIST HR. Interleukin-33 in health and disease[J]. Nat Rev Immunol, 2016, 16(11): 676-689. DOI: 10.1038/nri.2016.95.
    [13] FERHAT M, ROBIN A, GIRAUD S, et al. Endogenous IL-33 contributes to kidney ischemia-reperfusion injury as an alarmin[J]. J Am Soc Nephrol, 2018, 29(4): 1272-1288. DOI: 10.1681/ASN.2017060650.
    [14] LIANG H, XU F, WEN XJ, et al. Interleukin-33 signaling contributes to renal fibrosis following ischemia reperfusion[J]. Eur J Pharmacol, 2017, 812: 18-27. DOI: 10.1016/j.ejphar.2017.06.031.
    [15] AZIZ M, BRENNER M, WANG P. Extracellular CIRP (eCIRP) and inflammation[J]. J Leukoc Biol, 2019, 106(1): 133-146. DOI: 10.1002/JLB.3MIR1118-443R.
    [16] CEN C, MCGINN J, AZIZ M, et al. Deficiency in cold-inducible RNA-binding protein attenuates acute respiratory distress syndrome induced by intestinal ischemia-reperfusion[J]. Surgery, 2017, 162(4): 917-927. DOI: 10.1016/j.surg.2017.06.004.
    [17] CEN C, YANG WL, YEN HT, et al. Deficiency of cold-inducible ribonucleic acid-binding protein reduces renal injury after ischemia-reperfusion[J]. Surgery, 2016, 160(2): 473-483. DOI: 10.1016/j.surg.2016.04.014.
    [18] FANG C, WEI X, WEI Y. Mitochondrial DNA in the regulation of innate immune responses[J]. Protein Cell, 2016, 7(1): 11-16. DOI: 10.1007/s13238-015-0222-9.
    [19] HU Q, WOOD CR, CIMEN S, et al. Mitochondrial damage-associated molecular patterns (MTDs) are released during hepatic ischemia reperfusion and induce inflammatory responses[J]. PLoS One, 2015, 10(10): e0140105. DOI: 10.1371/journal.pone.0140105.
    [20] HU Q, REN H, REN J, et al. Released mitochondrial DNA following intestinal ischemia reperfusion induces the inflammatory response and gut barrier dysfunction[J]. Sci Rep, 2018, 8(1): 7350. DOI: 10.1038/s41598-018-25387-8.
    [21] KIM SW, LEE H, LEE HK, et al. Neutrophil extracellular trap induced by HMGB1 exacerbates damages in the ischemic brain[J]. Acta Neuropathol Commun, 2019, 7(1): 94. DOI: 10.1186/s40478-019-0747-x.
    [22] WANG S, XIE T, SUN S, et al. DNase-1 treatment exerts protective effects in a rat model of intestinal ischemia-reperfusion injury[J]. Sci Rep, 2018, 8(1): 17788. DOI: 10.1038/s41598-018-36198-2.
    [23] TSAI YF, YU HP, CHANG WY, et al. Sirtinol inhibits neutrophil elastase activity and attenuates lipopolysaccharide-mediated acute lung injury in mice[J]. Sci Rep, 2015, 5: 8347. DOI: 10.1038/srep08347.
    [24] GE L, ZHOU X, JI WJ, et al. Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow: therapeutic potential of DNase-based reperfusion strategy[J]. Am J Physiol Heart Circ Physiol, 2015, 308(5): H500-H509. DOI: 10.1152/ajpheart.00381.2014.
    [25] DUCROUX C, DI MEGLIO L, LOYAU S, et al. Thrombus neutrophil extracellular traps content impair tPA-induced thrombolysis in acute ischemic stroke[J]. Stroke, 2018, 49(3): 754-757. DOI: 10.1161/STROKEAHA.117.019896.
    [26] STARK K, PHILIPPI V, STOCKHAUSEN S, et al. Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice[J]. Blood, 2016, 128(20): 2435-2449. DOI: 10.1182/blood-2016-04-710632.
    [27] BRINKMANN V. Neutrophil extracellular traps in the second decade[J]. J Innate Immun, 2018, 10(5/6): 414-421. DOI: 10.1159/000489829.
    [28] 陈玲, 胡阳, 王煜, 等. 远程缺血预处理-减轻心肌再灌注损伤的机制[J]. 实用医学杂志, 2021, 37(1): 121-124. DOI: 10.3969/j.issn.1006-5725.2021.01.025.

    CHEN L, HU Y, WANG Y, et al. Mechanism of remote ischemic preconditioning to reduce myocardial reperfusion injury[J]. J Pract Med, 2021, 37(1): 121-124. DOI: 10.3969/j.issn.1006-5725.2021.01.025.
    [29] HAYASE N, DOIK, HIRUMA T, et al. Recombinant thrombomodulin prevents acute lung injury induced by renal ischemia-reperfusion injury[J]. Sci Rep, 2020, 10(1): 289. DOI: 10.1038/s41598-019-57205-0.
    [30] ZHANG H, GOSWAMI J, VARLEY P, et al. Hepatic surgical stress promotes systemic immunothrombosis that results in distant organ injury[J]. Front Immunol, 2020, 11: 987. DOI: 10.3389/fimmu.2020.00987.
    [31] LEWIS HD, LIDDLE J, COOTE JE, et al. Inhibition of PAD4 activity is sufficient to disrupt mouse and human NET formation[J]. Nat Chem Biol, 2015, 11(3): 189-191. DOI: 10.1038/nchembio.1735.
    [32] ZHANG S, ZHANG Q, WANG F, et al. Hydroxychloroquine inhibiting neutrophil extracellular trap formation alleviates hepatic ischemia/reperfusion injury by blocking TLR9 in mice[J]. Clin Immunol, 2020, 216: 108461. DOI: 10.1016/j.clim.2020.108461.
    [33] YAZDANI HO, CHEN HW, TOHME S, et al. IL-33 exacerbates liver sterile inflammation by amplifying neutrophil extracellular trap formation[J]. J Hepatol, 2017: S0168-8278(17)32291-2. DOI: 10.1016/j.jhep.2017.09.010.
    [34] MALLAVIA B, LIU F, LEFRANÇAIS E, et al. Mitochondrial DNA stimulates TLR9-dependent neutrophil extracellular trap formation in primary graft dysfunction[J]. Am J Respir Cell Mol Biol, 2020, 62(3): 364-372. DOI: 10.1165/rcmb.2019-0140OC.
    [35] MUTUA V, GERSHWIN LJ. A review of neutrophil extracellular traps (NETs) in disease: potential anti-NETs therapeutics[J]. Clin Rev Allergy Immunol, 2021, 61(2): 194-211. DOI: 10.1007/s12016-020-08804-7.
    [36] EDWARDS NJ, HWANG C, MARINI S, et al. The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury[J]. FASEB J, 2020, 34(12): 15753-15770. DOI: 10.1096/fj.202000994RR.
    [37] SCOZZI D, WANG X, LIAO F, et al. Neutrophil extracellular trap fragments stimulate innate immune responses that prevent lung transplant tolerance[J]. Am J Transplant, 2019, 19(4): 1011-1023. DOI: 10.1111/ajt.15163.
    [38] ZINDEL J, KUBES P. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation[J]. Annu Rev Pathol, 2020, 15: 493-518. DOI: 10.1146/annurev-pathmechdis-012419-032847.
  • 加载中
图(1)
计量
  • 文章访问数:  426
  • HTML全文浏览量:  295
  • PDF下载量:  103
  • 被引次数: 0
出版历程
  • 收稿日期:  2021-07-06
  • 刊出日期:  2021-11-15

目录

    /

    返回文章
    返回