[1] |
Hikichi M, Mizumura K, Maruoka S, et al. Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke[J]. Journal of Thoracic Disease, 2019, 11(S17): S2129 – S2140. doi: 10.21037/jtd.2019.10.43
|
[2] |
Cipollina C, Bruno A, Fasola S, et al. Cellular and molecular signatures of oxidative stress in bronchial epithelial cell models injured by cigarette smoke extract[J]. International Journal of Molecular Sciences, 2022, 23(3): 1770. doi: 10.3390/ijms23031770
|
[3] |
GBD Chronic Respiratory Disease Collaborators. Prevalence and attributable health burden of chronic respiratory diseases, 1990 – 2017: a systematic analysis for the Global Burden of Disease Study 2017[J]. The Lancet Respiratory Medicine, 2020, 8(6): 585 – 596. doi: 10.1016/S2213-2600(20)30105-3
|
[4] |
Liu AB, Zhang X, Li RG, et al. Overexpression of the SARS-CoV-2 receptor ACE2 is induced by cigarette smoke in bronchial and alveolar epithelia[J]. The Journal of Pathology, 2021, 253(1): 17 – 30. doi: 10.1002/path.5555
|
[5] |
刘佳莉, 丁甘玲, 汪嘉琦, 等. 穿心莲内酯对香烟烟雾诱导小鼠肺损伤拮抗作用[J]. 中国公共卫生, 2022, 38(5): 585 – 588. doi: 10.11847/zgggws1136848
|
[6] |
Mossina A, Lukas C, Merl-Pham J, et al. Cigarette smoke alters the secretome of lung epithelial cells[J]. Proteomics, 2017, 17(1/2): 1600243.
|
[7] |
Kubo H. Extracellular vesicles in lung disease[J]. Chest, 2018, 153(1): 210 – 216. doi: 10.1016/j.chest.2017.06.026
|
[8] |
Gomez N, James V, Onion D, et al. Extracellular vesicles and chronic obstructive pulmonary disease (COPD): a systematic review[J]. Respiratory Research, 2022, 23(1): 82. doi: 10.1186/s12931-022-01984-0
|
[9] |
O’Farrell HE, Yang IA. Extracellular vesicles in chronic obstructive pulmonary disease (COPD)[J]. Journal of Thoracic Disease, 2019, 11(S17): S2141 – S2154. doi: 10.21037/jtd.2019.10.16
|
[10] |
Brightling C, Greening N. Airway inflammation in COPD: progress to precision medicine[J]. European Respiratory Journal, 2019, 54(2): 1900651. doi: 10.1183/13993003.00651-2019
|
[11] |
Lu Z, Van Eeckhoutte HP, Liu G, et al. Necroptosis signaling promotes inflammation, airway remodeling, and emphysema in chronic obstructive pulmonary disease[J]. American Journal of Respiratory and Critical Care Medicine, 2021, 204(6): 667 – 681. doi: 10.1164/rccm.202009-3442OC
|
[12] |
Dang XM, He BB, Ning Q, et al. Alantolactone suppresses inflammation, apoptosis and oxidative stress in cigarette smoke-induced human bronchial epithelial cells through activation of Nrf2/HO-1 and inhibition of the NF-κB pathways[J]. Respiratory Research, 2020, 21(1): 95. doi: 10.1186/s12931-020-01358-4
|
[13] |
Racanelli AC, Kikkers SA, Choi AMK, et al. Autophagy and inflammation in chronic respiratory disease[J]. Autophagy, 2018, 14(2): 221 – 232. doi: 10.1080/15548627.2017.1389823
|
[14] |
Miao Q, Xu YF, Zhang HN, et al. Cigarette smoke induces ROS mediated autophagy impairment in human corneal epithelial cells[J]. Environmental Pollution, 2019, 245: 389 – 397. doi: 10.1016/j.envpol.2018.11.028
|
[15] |
McGuinness AJ, Sapey E. Oxidative stress in COPD: sources, markers, and potential mechanisms[J]. Journal of Clinical Medicine, 2017, 6(2): 21. doi: 10.3390/jcm6020021
|
[16] |
Yang DQ, Zuo QN, Wang T, et al. Mitochondrial-targeting antioxidant SS-31 suppresses airway inflammation and oxidative stress induced by cigarette smoke[J]. Oxidative Medicine and Cellular Longevity, 2021, 2021: 6644238.
|
[17] |
Liu XM, Ma YM, Luo LJ, et al. Dihydroquercetin suppresses cigarette smoke induced ferroptosis in the pathogenesis of chronic obstructive pulmonary disease by activating Nrf2-mediated path-way[J]. Phytomedicine, 2022, 96: 153894. doi: 10.1016/j.phymed.2021.153894
|
[18] |
Aspera-Werz RH, Ehnert S, Heid D, et al. Nicotine and cotinine inhibit catalase and glutathione reductase activity contributing to the impaired osteogenesis of SCP-1 cells exposed to cigarette smoke[J]. Oxidative Medicine and Cellular Longevity, 2018, 2018: 3172480.
|
[19] |
Remigante A, Morabito R. Cellular and molecular mechanisms in oxidative stress-related diseases[J]. International Journal of Mole-cular Sciences, 2022, 23(14): 8017. doi: 10.3390/ijms23148017
|
[20] |
Lakshmi SP, Reddy AT, Kodidhela LD, et al. Epigallocatechin gallate diminishes cigarette smoke-induced oxidative stress, lipid peroxidation, and inflammation in human bronchial epithelial cells[J]. Life Sciences, 2020, 259: 118260. doi: 10.1016/j.lfs.2020.118260
|
[21] |
王炳南, 张景熙, 白冲. 细胞衰老与慢性阻塞性肺疾病相关性研究进展[J]. 中华结核和呼吸杂志, 2021, 44(1): 59 – 63. doi: 10.3760/cma.j.cn112147-20200203-00047
|
[22] |
Araya J, Tsubouchi K, Sato N, et al. PRKN-regulated mitophagy and cellular senescence during COPD pathogenesis[J]. Autophagy, 2019, 15(3): 510 – 526. doi: 10.1080/15548627.2018.1532259
|
[23] |
Woldhuis RR, de Vries M, Timens W, et al. Link between increased cellular senescence and extracellular matrix changes in COPD[J]. American Journal of Physiology-Lung Cellular and Molecular Physiology, 2020, 319(1): L48 – L60. doi: 10.1152/ajplung.00028.2020
|
[24] |
Guan RJ, Wang J, Cai Z, et al. Hydrogen sulfide attenuates cigarette smoke-induced airway remodeling by upregulating SIRT1 signaling pathway[J]. Redox Biology, 2020, 28: 101356. doi: 10.1016/j.redox.2019.101356
|
[25] |
Kadota T, Fujita Y, Yoshioka Y, et al. Extracellular vesicles in chronic obstructive pulmonary disease[J]. International Journal of Molecular Sciences, 2016, 17(11): 1801. doi: 10.3390/ijms17111801
|
[26] |
Ishikawa S, Matsumura K, Kitamura N, et al. Multi-omics analysis: repeated exposure of a 3D bronchial tissue culture to whole-cigarette smoke[J]. Toxicology in Vitro, 2019, 54: 251 – 262. doi: 10.1016/j.tiv.2018.10.001
|
[27] |
Eapen MS, Lu WY, Hackett TL, et al. Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial-mesenchymal transition[J]. ERJ Open Research, 2021, 7(2): 00876 – 2020.
|
[28] |
Barnes PJ. Inflammatory mechanisms in patients with chronic obstructive pulmonary disease[J]. Journal of Allergy and Clinical Immunology, 2016, 138(1): 16 – 27. doi: 10.1016/j.jaci.2016.05.011
|
[29] |
Ryu AR, Kim DH, Kim E, et al. The potential roles of extracellular vesicles in cigarette smoke-associated diseases[J]. Oxidative Medicine and Cellular Longevity, 2018, 2018: 4692081.
|
[30] |
Cordazzo C, Petrini S, Neri T, et al. Rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke is dependent on Ca2+ mobilization[J]. Inflammation Research, 2014, 63(7): 539 – 547. doi: 10.1007/s00011-014-0723-7
|
[31] |
Moon HG, Kim SH, Gao JM, et al. CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke[J]. American Journal of Physiology-Lung Cellular and Molecular Physiology, 2014, 307(4): L326 – L337. doi: 10.1152/ajplung.00102.2014
|
[32] |
Chen Y, Li GP, Liu YX, et al. Translocation of endogenous danger signal HMGB1 from nucleus to membrane microvesicles in macrophages[J]. Journal of Cellular Physiology, 2016, 231(11): 2319 – 2326. doi: 10.1002/jcp.25352
|
[33] |
Sheller S, Papaconstantinou J, Urrabaz-Garza R, et al. Amnion-epithelial-cell-derived exosomes demonstrate physiologic state of cell under oxidative stress[J]. PLoS One, 2016, 11(6): e0157614. doi: 10.1371/journal.pone.0157614
|
[34] |
Ismail N, Wang YJ, Dakhlallah D, et al. Macrophage microvesicles induce macrophage differentiation and miR-223 transfer[J]. Blood, 2013, 121(6): 984 – 995. doi: 10.1182/blood-2011-08-374793
|
[35] |
Ramírez-Hernández AA, Velázquez-Enríquez JM, Santos-Álvarez JC, et al. The role of extracellular vesicles in idiopathic pulmonary fibrosis progression: an approach on their therapeutics potential[J]. Cells, 2022, 11(4): 630. doi: 10.3390/cells11040630
|
[36] |
Héliot A, Landkocz Y, Saint-Georges FR, et al. Smoker extracellular vesicles influence status of human bronchial epithelial cells[J]. International Journal of Hygiene and Environmental Health, 2017, 220(2): 445 – 454. doi: 10.1016/j.ijheh.2016.12.010
|
[37] |
Benedikter BJ, Weseler AR, Wouters EFM, et al. Redox-dependent thiol modifications: implications for the release of extracellular vesicles[J]. Cellular and Molecular Life Sciences, 2018, 75(13): 2321 – 2337. doi: 10.1007/s00018-018-2806-z
|
[38] |
Xu H, Ling M, Xue JC, et al. Exosomal microRNA-21 derived from bronchial epithelial cells is involved in aberrant epithelium-fibroblast cross-talk in COPD induced by cigarette smoking[J]. Theranostics, 2018, 8(19): 5419 – 5433. doi: 10.7150/thno.27876
|
[39] |
Fujita Y, Araya J, Ito S, et al. Suppression of autophagy by extracellular vesicles promotes myofibroblast differentiation in COPD pathogenesis[J]. Journal of Extracellular Vesicles, 2015, 4(1): 28388. doi: 10.3402/jev.v4.28388
|
[40] |
Finicelli M, Digilio FA, Galderisi U, et al. The emerging role of macrophages in chronic obstructive pulmonary disease: the potential impact of oxidative stress and extracellular vesicle on macrophage polarization and function[J]. Antioxidants (Basel), 2022, 11(3): 464. doi: 10.3390/antiox11030464
|
[41] |
陈圳, 苏薇薇, 王永刚, 等. 细胞外囊泡在慢性阻塞性肺疾病中的作用[J]. 生理科学进展, 2021, 52(6): 466 – 470. doi: 10.3969/j.issn.0559-7765.2021.06.013
|