|本期目录/Table of Contents|

[1]孔凯文,孟岩,邓小明.Nrf2/HO-1信号通路在急性肺损伤中的研究进展[J].医学研究与战创伤救治(原医学研究生学报),2022,24(6):646-651.[doi:10.3969/j.issn.1672-271X.2022.06.017]
 KONG Kai-wen,MENG Yan,DENG Xiao-ming.Research progress of Nrf2/HO-1 signaling pathway in acute lung injury[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2022,24(6):646-651.[doi:10.3969/j.issn.1672-271X.2022.06.017]
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Nrf2/HO-1信号通路在急性肺损伤中的研究进展()

《医学研究与战创伤救治》(原医学研究生学报)[ISSN:1672-271X/CN:32-1713/R]

卷:
第24卷
期数:
2022年6期
页码:
646-651
栏目:
综述
出版日期:
2023-01-18

文章信息/Info

Title:
Research progress of Nrf2/HO-1 signaling pathway in acute lung injury
作者:
孔凯文孟岩邓小明
作者单位:200433上海,海军军医大学(第二军医大学)第一附属医院麻醉科(孔凯文、孟岩、邓小明)
Author(s):
KONG Kai-wen MENG Yan DENG Xiao-ming
(Department of Anesthesiology, The First Affiliated Hospital of Naval Medical University/Second Military Medical University, Shanghai 200433, China)
关键词:
核因子E2相关因子2血红素加氧酶-1急性肺损伤急性呼吸窘迫综合征
Keywords:
nuclear factor E2-related factor 2heme oxygenase-1acute lung injuryacute respiratory distress syndrome
分类号:
R563
DOI:
10.3969/j.issn.1672-271X.2022.06.017
文献标志码:
A
摘要:
核因子E2相关因子2(Nrf2)是细胞内一种重要的转录因子,被激活后可促进其下游血红素加氧酶-1(HO-1)的表达。HO-1是血红素降解过程的限速酶,能够催化血红素降解为胆绿素、Fe2+和一氧化碳。由于HO-1及其催化产物具有显著的抗氧化和抗炎作用,近些年受到越来越多的关注。最近研究发现,Nrf2/HO-1信号通路在急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)中能够减轻炎症反应和氧化应激损伤,抑制细胞焦亡和铁死亡,进而减轻肺损伤。文章就Nrf2/HO-1信号通路在ALI/ARDS的最新研究成果进行综述。
Abstract:
Nuclear factor E2-related factor 2 (Nrf2) is a key transcription factor in cells, which can promote the expression of its downstream heme oxygenase-1 (HO-1) when activated. HO-1 is the rate-limiting enzyme in the degradation process of heme, which can catalyze the degradation of heme into biliverdin, Fe2+ and carbon monoxide. HO-1 and its catalytic products have received more and more attention in recent years due to their significant antioxidant and anti-inflammatory effects. Recent studies have found that Nrf2/HO-1 signaling pathway in ALI/ARDS can reduce the inflammatory response and oxidative stress injury, inhibit cell pyroptosis and ferroptosis, and then reduce lung injury. This article describes the latest research results of Nrf2/HO-1 signaling pathway in ALI/ARDS, in order to provide new therapeutic ideas.

参考文献/References:

[1]Meyer NJ, Gattinoni L, Calfee CS. Acute respiratory distress syndrome[J].Lancet, 2021,398(10300):622-637.
[2]Matthay MA, Zemans RL, Zimmerman GA, et al. Acute respiratory distress syndrome[J].Nat Rev Dis Primers, 2019,5(1):18.
[3]Chen QM. Nrf2 for cardiac protection: pharmacological options against oxidative stress[J]. Trends Pharmacol Sci, 2021,42(9):729-744.
[4]Campbell NK, Fitzgerald HK, Dunne A. Regulation of inflammation by the antioxidant haem oxygenase 1[J]. Nat Rev Immunol, 2021,21(7):411-425.
[5]Ashbaugh D, Bigelow DB, Petty T, et al. Acute respiratory distress in adults[J]. Lancet, 1967, 290(7511):319-323.
[6]Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination[J]. J Crit Care, 1994, 9(1):72-81.
[7]ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition[J]. Jama, 2012,307(23):2526-2533.
[8]Xu G, Wan H, Yi L, et al. Berberine administrated with different routes attenuates inhaled LPS-induced acute respiratory distress syndrome through TLR4/NF-κB and JAK2/STAT3 inhibition[J]. Eu J Pharmacol, 2021(1):174349.
[9]Hazeldine J, Lord JM. Neutrophils and COVID-19: Active Participants and Rational Therapeutic Targets[J]. Front Immunol,2021, 12:680134.
[10]Imai Y, Parodo J, Kajikawa O, et al. Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome[J]. JAMA, 2003, 289(16):2104-2112.
[11]Frye M, Dierkes M, Küppers V, et al. Interfering with VE-PTP stabilizes endothelial junctions in vivo via Tie-2 in the absence of VE-cadherin[J]. J Exp Med,2015, 2015:2267-2287.
[12]Shaver CM, Wickersham N, Mcneil JB, et al. Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury[J]. Jci Insight, 2018, 3(2):e98546.
[13]Mekontso Dessap A, Gendreau S, Vieillard-Baron A. Respective roles of hypercapnia and acidosis in acute distress respiratory syndrome[J]. Intensive Care Med,2022,48(6):787-788.
[14]Gwozdzinska P, Buchbinder BA, Mayer K. Hypercapnia impairs ENaC cell surface by promoting phosphorylation, polyubiquitination and endocytosis of β-ENaC in a human alveolar epithelial cell line[J]. Front Immunol,2017,8:591.
[15]Vohwinkel CU, Lecuona E, Sun H, et al. Elevated CO2 Levels Cause Mitochondrial Dysfunction and Impair Cell Proliferation[J]. J Biol Chem, 2011, 286(43):37067-37076.
[16]Tong KI, Katoh Y, Kusunoki H, et al. Keap1 Recruits Neh2 through Binding to ETGE and DLG Motifs: Characterization of the Two-Site Molecular Recognition Model[J]. Mol Cell Biol, 2006, 26(8):2887-2900.
[17]Zhang DD, Lo SC, Cross JV, et al. Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex[J]. Mol Cell Biol, 2004, 24(24):10941-10953.
[18]Dinkova-Kostova AT, Kostov RV, Canning P. Keap1, the cysteine-based mammalian intracellular sensor for electrophiles and oxidants[J]. Arch Biochem Biophys, 2017, 617:84-93.
[19]Horie Y, Suzuki T, Inoue J, et al. Molecular basis for the disruption of Keap1-Nrf2 interaction via Hinge & Latch mechanism[J]. Commun Biol,2021,4(1):576.
[20]Jiang T, Harder B, Rojo de la Vega M, et al. p62 links autophagy and Nrf2 signaling[J]. Free Radic Biol Med, 2015, 88(Pt.B):199-204.
[21]Ichimura Y, Waguri S, Sou YS, et al. Phosphorylation of p62 Activates the Keap1-Nrf2 Pathway during Selective Autophagy[J]. Mol Cell, 2013, 51(5):618-631.
[22]Itoh K, Chiba T, Takahashi S, et al. An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements[J]. Biochem Biophys Res Commun, 1997, 236(2):313-322.
[23]Kunutsor SK, Bakker SJL, Gansevoort RT, et al. Circulating Total Bilirubin and Risk of Incident Cardiovascular Disease in the General Population[J]. Arterioscler Thromb Vasc Biol, 2015, 35(3):716-724.
[24]Yachie A, Varga Z, Jacob HS, et al. Heme, heme oxygenase, and ferritin: how the vascular endothelium survives (and dies) in an iron-rich environment[J]. Antioxid Redox Signal, 2007, 9(12):2119-2137.
[25]Ryter SW, Choi A. Targeting heme oxygenase-1 and carbon monoxide for therapeutic modulation of inflammation[J]. Transl Res, 2016, 167(1):7.
[26]Lee W, Chang HL, Lee J, et al. Botanical formulation, TADIOS, alleviates lipopolysaccharide (LPS)-Induced acute lung injury in mice via modulation of the Nrf2-HO-1 signaling pathway-Science Direct[J]. J Ethnopharmacol, 2021,270:113795.
[27]Huang J, Fan R, Zou Y, et al. Salviplenoid A from Salvia plebeia attenuates acute lung inflammation via modulating NF‐κB and Nrf2 signaling pathways[J]. Phytother Res, 2021,35(3):1559-1571.
[28]Bi XG, Li ML, Xu W, et al. Helix B surface peptide protects against acute lung injury through reducing oxidative stress and endoplasmic reticulum stress via activation of Nrf2/HO-1 signaling pathway[J].Eur Rev Med Pharmacol Sci,2020,24(12):6919-6930.
[29]Liu Y, Zhou J, Luo Y, et al. Honokiol alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via Nrf2 activation in vitro and in vivo[J]. Chin Med, 2021,16(1):127.
[30]Li J, Lu K, Sun F, et al. Panaxydol attenuates ferroptosis against LPS-induced acute lung injury in mice by Keap1-Nrf2/HO-1 pathway[J]. J Trans Med, 2021, 19(1):96.
[31]Gao D, Liu F, Li Z, et al. Isobavachalcone attenuates Sephadex-induced lung injury via activation of A20 and NRF2/HO-1 in rats[J]. Eur J Pharmacol, 2019,848:49-54.
[32]Xu JQ, Li H, Chen L,et al. BML-111 accelerates the resolution of inflammation by modulating the Nrf2/HO-1 and NF-κB pathways in rats with ventilator-induced lung injury[J]. Int immunopharmacol, 2019,69:289-298.
[33]Lin F, Xiao J, Liang F, et al. Preconditioning with rHMGB1 ameliorates lung ischemia-reperfusion injury by inhibiting alveolar macrophage pyroptosis via the Keap1/Nrf2/HO-1 signaling pathway[J].Transl Med,2020,18(1):301.
[34]Qiu YB, Wan BB, Liu G, et al. Nrf2 protects against drowning-induced acute lung injury via inhibiting ferroptosis[J].Respir Res,2020,21(1):232.
[35]Xqsa B, Chen WA, Ybq A, et al. Heme oxygenase-1 attenuates seawater drowning-induced acute lung injury through a reduction in inflammation and oxidative stress-ScienceDirect[J]. Int Immunopharmacol, 2019,74:105634.
[36]Yu Y, Yang Y, Yang M, et al. Hydrogen gas reduces HMGB1 release in lung tissues of septic mice in an Nrf2/HO-1-dependent pathway[J]. Int Immunopharmacol, 2019, 69:11-18.
[37]Gao Z, Sui J, Fan R, et al. Emodin Protects Against Acute Pancreatitis-Associated Lung Injury by Inhibiting NLPR3 Inflammasome Activation via Nrf2/HO-1 Signaling[J]. Drug Des Devel Ther, 2020, 14:1971-1982.
[38]Dong H, Qiang Z, Chai D, et al. Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1[J]. Aging (Albany NY), 2020,12(13):12943-12959.
[39]Fan JH, Lv H, Li J, et al. Roles of Nrf2/HO-1 and HIF-1α/VEGF in lung tissue injury and repair following cerebral ischemia/reperfusion injury[J]. J Cell Physiol, 2019, 234(6):7695-7077.

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备注/Memo

备注/Memo:
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更新日期/Last Update: 2023-01-18