细胞程序性坏死在急性肺损伤中作用的研究进展

王亚丽, 朱蕾

复旦学报(医学版) ›› 2021, Vol. 48 ›› Issue (03) : 393-397.

PDF(696 KB)
欢迎访问《复旦学报(医学版)》官方网站,今天是 2025年6月28日 星期六 分享到:
PDF(696 KB)
复旦学报(医学版) ›› 2021, Vol. 48 ›› Issue (03) : 393-397. DOI: 10.3969/j.issn.1672-8467.2021.03.018
综述

细胞程序性坏死在急性肺损伤中作用的研究进展

  • 王亚丽, 朱蕾
作者信息 +

Research progresses on the role of necroptosis in acute lung injury

  • WANG Ya-li, ZHU Lei
Author information +
文章历史 +

摘要

程序性坏死作为一种新的细胞程序性死亡方式参与急性肺损伤(acute lung injury,ALI)的病理过程,主要在疾病前期由各类高危因素触发,由受体相互作用蛋白激酶1(receptor-interacting protein kinase 1,RIPK1)、RIPK3、混合谱系激酶结构域样蛋白(mixed-lineage kinase domain-like protein,MLKL)介导,导致肺泡上皮细胞、血管内皮细胞、肺泡巨噬细胞等细胞死亡,直接或通过调节机体炎症反应造成严重的肺泡结构损伤及肺水肿,应用抑制剂阻断程序性坏死可以减轻肺损伤。本文就程序性坏死在ALI中的作用进行综述,以期为临床筛选高危患者和治疗提供依据。

Abstract

A newly reported programmed cell death, necroptosis,is involved in the pathological process of acute lung injury (ALI).Necroptosis is triggered in early stage of the disease under several high risk factors and mainly mediated by receptor interacting protein kinase 1 (RIPK1),RIPK3,and mixed lineage kinase domain-like proteins (MLKL).Necroptosis of alveolar epithelial cells,vascular endothelial cells,alveolar macrophages and other cells causes severe alveolar injury and edema directly or by regulating inflammatory response.The application of inhibitors to block necroptosis can reduce lung injury.This review summarizes the role of necroptosis in ALI to provide information to screen high-risk patients and therapy.

引用本文

导出引用
王亚丽, 朱蕾. 细胞程序性坏死在急性肺损伤中作用的研究进展[J]. 复旦学报(医学版), 2021, 48(03): 393-397 https://doi.org/10.3969/j.issn.1672-8467.2021.03.018
WANG Ya-li, ZHU Lei. Research progresses on the role of necroptosis in acute lung injury[J]. Fudan University Journal of Medical Sciences, 2021, 48(03): 393-397 https://doi.org/10.3969/j.issn.1672-8467.2021.03.018
中图分类号: R563.8   

参考文献

[1] MATTHAY MA,ZEMANS RL,ZIMMERMAN GA,et al.Acute respiratory distress syndrome[J].Nat Rev Dis Primers,2019,5(1):18.
[2] GROOTJANS S,VANDEN BERGHE T,VANDENA-BEELE P.Initiation and execution mechanisms of necroptosis:an overview[J].Cell Death Differ,2017,24(7):1184-1195.
[3] 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.
[4] SHAN B,PAN H.Necroptosis in development and diseases[J].Genes Dev,2018,32(5-6):327-340.
[5] CHEN J,WANG S,FU R,et al.RIP3 dependent NLRP3 inflammasome activation is implicated in acute lung injury in mice[J].J Transl Med,2018,16(1):233.
[6] TONNUS W,MEYER C,PALIEGE A,et al.The pathological features of regulated necrosis[J].J Pathol,2019,247(5):697-707.
[7] QING DY,CONEGLIANO D,SHASHATY MG,et al.Red blood cells induce necroptosis of lung endothelial cells and increase susceptibility to lung inflammation[J].Am J Respir Crit Care Med,2014,190(11):1243-1254.
[8] FERRARI RS,ANDRADE CF.Oxidative stress and lung ischemia-reperfusion injury[J].Oxid Med Cell Longev,2015,2015:590987.
[9] SIEMPOS II,MA KC,IMAMURA M,et al.RIPK3 mediates pathogenesis of experimental ventilator-induced lung injury[J].JCI Insight,2018,3(9):e97102.
[10] PAN L,YAO DC,YU YZ,et al.Necrostatin-1 protects against oleic acid-induced acute respiratory distress syndrome in rats[J].Biochem Biophys Res Commun,2016,478(4):1602-1608.
[11] HAN CH,GUAN Z,ZHANG PX,et al.Oxidative stress induced necroptosis activation is involved in the pathogenesis of hyperoxic acute lung injury[J].Biochem Biophys Res Commun,2018,495(3):2178-2183.
[12] TAMADA N,TOJO K,YAZAWA T,et al.Necrosis rather than apoptosis is the dominant form of alveolar epithelial cell death in lipopolysaccharide-induced experimental acute respiratory distress syndrome model[J].Shock,2019,54(1):128-139.
[13] SULIMAN HB,KRAFT B,BARTZ R,et al.Mitochondrial quality control in alveolar epithelial cells damaged by S.aureus pneumonia in mice[J].Am J Physiol Lung Cell Mol Physiol,2017,313(4):L699-L709.
[14] WEN SH,LIN LN,WU HJ,et al.TNF-α increases Staphylococcus aureus-induced death of human alveolar epithelial cell line A549 associated with RIP3-mediated necroptosis[J].Life Sci,2018,195:81-86.
[15] WANG Y,HAO Q,FLORENCE JM,et al.Influenza virus infection induces ZBP1 expression and necroptosis in mouse lungs[J].Front Cell Infect Microbiol,2019,9:286.
[16] ZHAO H,NING J,LEMAIRE A,et al.Necroptosis and parthanatos are involved in remote lung injury after receiving ischemic renal allografts in rats[J].Kidney Int,2015,87(4):738-748.
[17] ZHAO H,CHEN Q,HUANG H,et al.Osteopontin mediates necroptosis in lung injury after transplantation of ischaemic renal allografts in rats[J].Br J Anaesth,2019,123(4):519-530.
[18] YU X,MAO M,LIU X,et al.A cytosolic heat shock protein 90 and co-chaperone p23 complex activates RIPK3/MLKL during necroptosis of endothelial cells in acute respiratory distress syndrome[J].J Mol Med (Berl),2020,98(4):569-583.
[19] DU XK,GE WY,JING R,et al.Necroptosis in pulmonary macrophages mediates lipopolysaccharide-induced lung inflammatory injury by activating ZBP-1[J].Int Immuno-pharmacol,2019,77:105944.
[20] CHEN H,LI Y,WU J,et al.RIPK3 collaborates with GSDMD to drive tissue injury in lethal polymicrobial sepsis[J].Cell Death Differ,2020,27(9):2568-2585.
[21] KITUR K,PARKER D,NIETO P,et al.Toxin-induced necroptosis is a major mechanism of Staphylococcus aureus lung damage[J].PLoS Pathog,2015,11(4):e1004820.
[22] LEE SH,SHIN JH,SONG JH,et al.Inhibition of insulin-like growth factor receptor-1 reduces necroptosis-related markers and attenuates LPS-induced lung injury in mice[J].Biochem Biophys Res Commun,2018,498(4):877-883.
[23] CAO M,CHEN F,XIE N,et al.c-Jun N-terminal kinases differentially regulate TNF-and TLRs-mediated necroptosis through their kinase-dependent and -independent activities[J].Cell Death Dis,2018,9(12):1140.
[24] WANG L,WANG T,LI H,et al.Receptor interacting protein 3-mediated necroptosis promotes lipopolysaccharide-induced inflammation and acute respiratory distress syndrome in mice[J].PLoS One,2016,11(5):e0155723.
[25] HAN CH,GUAN ZB,ZHANG PX,et al.Oxidative stress induced necroptosis activation is involved in the pathogenesis of hyperoxic acute lung injury[J].Biochem Biophys Res Commun,2018,495(3):2178-2183.
[26] KANOU T,OHSUMI A,KIM H,et al.Inhibition of regulated necrosis attenuates receptor-interacting protein kinase 1-mediated ischemia-reperfusion injury after lung transplantation[J].J Heart Lung Transplant,2018,37(10):1261-1270.
[27] WANG XG,O'Brien EM,YU J,et al.Prolonged cold ischemia induces necroptotic cell death in ischemia-reperfusion injury and contributes to primary Graft dysfunction after lung transplantation[J].Am J Respir Cell Mol Biol,2019,61(2):244-256.
[28] QIN C,SAI XY,QIAN XF,et al.Close relationship between cIAP2 and human ARDS induced by severe H7N9 infection[J].Biomed Res Int,2019,2019:2121357.
[29] KIM TH,HONG SB,LIM CM,et al.The role of exosomes in bronchoalveloar lavage from patients with acute respiratory distress syndrome[J].J Clin Med,2019,8(8):1148
[30] SHASHATY MGS,REILLY JP,FAUST HE,et al.Plasma receptor interacting protein kinase-3 levels are associated with acute respiratory distress syndrome in sepsis and trauma:a cohort study[J].Crit Care,2019,23(1):235.
[31] WANG M,ZHONG D,DONG P,et al.Blocking CXCR1/2 contributes to amelioration of lipopolysaccharide-induced sepsis by downregulating substance P[J].J Cell Biochem,2018,120(2):2007-2014.

基金

国家自然科学基金(81873420)
PDF(696 KB)

1511

Accesses

0

Citation

Detail

段落导航
相关文章

/