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中华细胞与干细胞杂志(电子版) ›› 2019, Vol. 09 ›› Issue (05) : 304 -308. doi: 10.3877/cma.j.issn.2095-1221.2019.05.008

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综述

Ⅱ型肺泡上皮细胞与特发性肺纤维化的关系研究进展
杨育坤1, 李晔1, 朱向情1, 雷银1, 王严影1, 田川1, 阮光萍1, 潘兴华1,()   
  1. 1. 652230 昆明,中国人民解放军联勤保障部队第920医院 干细胞与免疫细胞生物医药技术国家地方联合工程实验室 云南省细胞治疗技术转化医学重点实验室 云南省干细胞工程实验室 昆明医科大学
  • 收稿日期:2019-04-22 出版日期:2019-10-01
  • 通信作者: 潘兴华

Progress in the relationship between type II alveolar epithelial cells and idiopathic pulmonary fibrosis

Yukun Yang1, Ye Li1, Xiangqing Zhu1, Yin Lei1, Yanying Wang1, Chuan Tian1, Guangping Ruan1, Xinghua Pan1,()   

  1. 1. Yunnan Stem Cell Engineering Laboratory, Yunnan Provincial Key Laboratory of Cell Therapy and Translational Medicine, National and Local Joint Engineering Laboratory of Stem Cell and Immune Cell Biomedical Technology, 920th Hospital of Joint Logistics Support Force of PLA, Kunming Medical University, Kunming 652230 , China
  • Received:2019-04-22 Published:2019-10-01
  • Corresponding author: Xinghua Pan
  • About author:
    Corresponding author:Pan Xinghua, Email:
引用本文:

杨育坤, 李晔, 朱向情, 雷银, 王严影, 田川, 阮光萍, 潘兴华. Ⅱ型肺泡上皮细胞与特发性肺纤维化的关系研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2019, 09(05): 304-308.

Yukun Yang, Ye Li, Xiangqing Zhu, Yin Lei, Yanying Wang, Chuan Tian, Guangping Ruan, Xinghua Pan. Progress in the relationship between type II alveolar epithelial cells and idiopathic pulmonary fibrosis[J/OL]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2019, 09(05): 304-308.

特发性肺纤维化(IPF)是一种严重影响肺通气与换气功能的下呼吸道慢性疾病,其发病机理目前尚不明确,表现为异常的间质炎症和纤维化,以及肺泡结构的破坏。而Ⅱ型肺泡上皮细胞(ATⅡ)作为维持肺结构和功能的关键细胞,在肺部纤维化的发生和发展中极其重要。在IPF中,各种原因所致的ATⅡ的受损和衰老凋亡,可能是纤维化发生的是始动因素。而在这之后,关于临时基质的形成、成纤维细胞的聚集、激活以及间质-上皮转化的过程,异常的ATⅡ也参与其中,并发挥着重要的作用。

Pulmonary fibrosis is a chronic disease of the lower respiratory tract that seriously affects lung ventilation and ventilation. The pathogenesis is still unclear. It is characterized by abnormal interstitial inflammation and fibrosis, and destruction of alveolar structure. Type Ⅱ alveolar epithelial cells, as key cells of maintaining lung structure and function, are extremely important in the development and progression of pulmonary fibrosis. In pulmonary fibrosis, damage to typeⅡ alveolar epithelial cells and senescence apoptosis caused by various causes may be the initiation factors of pulmonary fibrosis. After that, abnormal typeⅡ alveolar epithelial cells are also involved and in the formation of temporary matrix, fibroblast aggregation, activation and interstitial-epithelial transformation, play an important role.

[1]
Beers MF, Moodley Y. When is an alveolar type 2 cell an alveolar type 2 cell? a conundrum for lung stem cell biology and regenerative medicine[J]. Am J Respir Cell Mol Biol, 2017, 57(1):18-27.
[2]
Guillot L, Nathan N, Tabary O, et al. Alveolar epithelial cells: master regulators of lung homeostasis[J]. Int J Biochem Cell Biol, 2013, 45(11):2568-2573.
[3]
Selman M, Thannickal VJ, Pardo A, et al. Idiopathic pulmonary fibrosis[J]. Semin Resp Crtt Care, 2011, 378(9807):1949.
[4]
Geiser T. Idiopathic pulmonary fibrosis - a disorder of alveolar wound repair?[J]. Swiss Med Wkly, 2003, 133(29/30):405-411.
[5]
Crapo JD, Young SL, Fram EK, et al. Morphometric characteristlcs of cells in the alveolar region of mammalian lungs[J]. Am Rev Respir Dis, 1983, 128(2 Pt 2):S42-46.
[6]
Baritussio AG, Magoon MW, Goerke J. Precursor-product relationship between rabbit typeⅡcell lamellar bodies and alveolar surface-active material.Surfactant turnover time[J]. Biochim Biophys Acta, 1981, 666(3):382-393.
[7]
Mason RJ. Biology of alveolar typeⅡcells[J]. Respirology, 2006, 11(S):S12-S15.
[8]
Lopez-Rodriguez E, Pérez-Gil J. Structure-function relationships in pulmonary surfactant membranes: From biophysics to therapy[J]. Biochim Biophys Acta, 2014, 1838(6):1568-1585.
[9]
Guth AM, Janssen WJ, Bosio CM, et al. Lung environment determines unique phenotype of alveolar macrophages[J]. Am J Physiol Lung Cell Mol Physiol, 2009, 296(6):L936-L946.
[10]
Hussell T, Bell TJ. Alveolar macrophages: plasticity in a tissue-specific context[J]. Nat Rev Immunol, 2014, 14(2):81-93.
[11]
O'Brien AD, Standiford TJ, Christensen PJ, et al. Chemotaxis of alveolar macrophages in response to signals derived from alveolar epithelial cells[J]. J Lab Clin Med,1998,131(5):417-424.
[12]
Fehrenbach H. Alveolar epithelial typeⅡcell: defender of the alveolus revisited[J]. Respir Res, 2001, 2(1):33-52.
[13]
Minoo P, King RJ. Epithelial-mesenchymal interactions in lung development[J]. Annu Rev Physiol, 1994, 56:13-45.
[14]
Haschek WM, Witschi H. Pulmonary fibrosis--a possible mechanism[J]. Toxicol Appl Pharmacol, 1979, 51(3):475-487.
[15]
Barbas-Filho JV, Ferreira MA, Sesso A, et al. Evidence of typeⅡ pneumocyte apoptosis in the pathogenesis of idiopathic pulmonary fibrosis(IFP)/usual interstitial pneumonia(UIP)[J]. J Clin Pathol, 2001, 54(2):132-138.
[16]
Sisson TH, Mendez M, Choi K, et al. Targeted injury of type II alveolar epithelial cells induces pulmonary fibrosis[J]. Am J Respir Crit Care Med, 2010, 181(3):254-263.
[17]
Tanjore H, Blackwell TS, Lawson WE. Emerging evidence for endoplasmic reticulum stress in the pathogenesis of idiopathic pulmonary fibrosis[J]. Am J Physiol Lung Cell Mol Physiol, 2012, 302(8):L721-L729.
[18]
Maitra M, Wang YY, Gerard RD, et al. Surfactant protein a2 mutations associated with pulmonary fibrosis Lead to protein instability and endoplasmic reticulum stress[J]. J Biol Chem, 2010, 285(29):22103-22113.
[19]
Nogee LM, Dunbar AE, Wert SE, et al. A mutation in the surfactant protein C gene associated with familial interstitial lung disease[J]. N Engl J Med, 2001, 344(8):573-579.
[20]
Lawson WE, Crossno PF, Polosukhin VV, et al. Endoplasmic reticulum stress in alveolar epithelial cells is prominent in IPF: association with altered surfactant protein processing and herpesvirus infection[J]. Am J Physiol Lung Cell Mol Physiol, 2008, 294(6):L1119-L1126.
[21]
Korfei M, Ruppert C, Mahavadi P, et al. Epithelial endoplasmic reticulum stress and apoptosis in sporadic idiopathic pulmonary fibrosis[J]. Am J Respir Crit Care Med, 2008, 178(8):838-846.
[22]
Mulugeta S, Nguyen V, Russo SJ, et al. A surfactant protein C precursor protein BRICHOS domain mutation causes endoplasmic reticulum stress, proteasome dysfunction, and caspase 3 activation[J]. Am J Respir Cell Mol Biol, 2005, 32(6):521-530.
[23]
Mulugeta S, Maguire JA, Newitt JL, et al. Misfolded BRICHOS SP-C mutant proteins induce apoptosis via caspase-4- and cytochrome c-related mechanisms[J]. Am J Physiol Lung Cell Mol Physiol, 2007, 293(3):L720-L729.
[24]
Lawson WE, Cheng DS, Degryse AL, et al. Endoplasmic reticulum stress enhances fibrotic remodeling in the lungs[J]. Proc Natl Acad Sci U S A, 2011, 108(26):10562-10567.
[25]
O'Dwyer DN, Ashley SL, Moore BB. Influences of innate immunity, autophagy and fibroblast activation in the pathogenesis of lung fibrosis[J]. Am J Physiol Lung Cell Mol Physiol, 2016, 11(3):L590-601.
[26]
Wang K, Zhang T, Lei YL, et al. Identification of ANXA2 (annexin A2) as a specific bleomycin target to induce pulmonary fibrosis by impeding TFEB-mediated autophagic flux[J]. Autophagy, 2018, 14(2):269-282.
[27]
Tomohiro Y, Usha N, Zhifen Y, et al. Endoplasmic reticulum stress triggers autophagy[J]. J Biol Chem, 2006, 281(40):30299-30304.
[28]
Bueno M, Lai YC, Romero Y, et al. PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis[J]. J Clin Invest, 2015, 125(2):521-538.
[29]
Birkelbach B, Lutz D, Ruppert C, et al. Linking progression of fibrotic lung remodeling and ultrastructural alterations of alveolar epithelial typeⅡcells in the amiodarone mouse model[J]. Am J Physiol Lung Cell Mol Physiol, 2015, 309(1):L63-L75.
[30]
Mahavadi P, Knudsen L, Venkatesan S, et al. Regulation of macroautophagy in amiodarone-induced pulmonary fibrosis[J]. J Pathol Clin Res, 2015, 1(4):252-263.
[31]
Armanios MY, Chen JJ, Cogan JD, et al. Telomerase mutations in families with idiopathic pulmonary fibrosis[J]. N Engl J Med, 2007, 356(13):1317-1326.
[32]
Tsakiri KD, Cronkhite JT, Kuan PJ, et al. Adult-onset pulmonary fibrosis caused by mutations in telomerase[J]. Proc Natl Acad Sci U S A, 2007, 104(18):7552-7557.
[33]
Camelo A, Dunmore R, Sleeman MA, et al. The epithelium in idiopathic pulmonary fibrosis: breaking the barrier[J]. Front Pharmacol, 2014, 4:173.
[34]
Caja L, Dituri F, Mancarella S, et al. TGF-β and the tissue microenvironment: relevance in fibrosis and cancer[J]. Int J Mol Sci, 2018, 19(5): pii: E1294.
[35]
Knudsen L, Lopez-Rodriguez E, Berndt L, et al. Pressure dependent alveolar derecruitment is linked with surfactant dysfunction in Bleomycin-Induced acute lung injury[J]. Am J Respir Crit Care Med, 2016, 193:A4813.
[36]
Knudsen L, Ruppert C, Ochs M. Tissue remodelling in pulmonary fibrosis[J]. Cell Tissue Res, 2017, 367(3):607-626.
[37]
Funke M, Zhao ZW, Xu Y, et al. The lysophosphatidic acid receptor LPA(1) promotes epithelial cell apoptosis after lung injury[J]. Am J Respir Cell Mol Biol, 2012, 46(3):355-364.
[38]
Wynn TA, Ramalingam TR. Mechanisms of fibrosis: therapeutic translation for fibrotic disease[J]. Nat Med, 2012, 18(7):1028-1040.
[39]
Richeldi L, Du Bois RM, Raghu G, et al. Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis[J]. N Engl J Med, 2014, 370(22):2071-2082.
[40]
Günther S, Bordenave J, Hua-Huy T, et al. Macrophage migration inhibitory factor (MIF) inhibition in a murine model of Bleomycin-Induced pulmonary fibrosis[J]. Int J Mol Sci, 2018, 19(12): pii: E4105.
[41]
Cao ZW, Lis R, Ginsberg M, et al. Targeting of the pulmonary capillary vascular niche promotes lung alveolar repair and ameliorates fibrosis[J]. Nat Med, 2016, 22(2):154-162.
[42]
Wynn TA. Integrating mechanisms of pulmonary fibrosis[J]. J Exp Med, 2011, 208(7):1339-1350.
[43]
Chambers RC. Procoagulant signalling mechanisms in lung inflammation and fibrosis: novel opportunities for pharmacological intervention?[J]. Br J Pharmacol, 2008, 153(Suppl 1):S367-S378.
[44]
Jagadapillai R, Rane MJ, Lin X, et al. Diabetic microvascular disease and pulmonary fibrosis: the contribution of platelets and systemic inflammation[J]. Int J Mol Sci, 2016, 17(11): pii: E1853.
[45]
Yang J, Wheeler SE, Velikoff M, et al. Activated alveolar epithelial cells initiate fibrosis through secretion of mesenchymal proteins[J]. Am J Pathol, 2013, 183(5):1559-1570.
[46]
Selman M, Pardo A. Role of epithelial cells in idiopathic pulmonary fibrosis:from innocent targets to serial killers[J]. Proc Am Thorac Soc, 2006, 3(4):364-372.
[47]
Andersson-Sjöland A, De Alba CG, Nihlberg K, et al. Fibrocytes are a potential source of lung fibroblasts in idiopathic pulmonary fibrosis[J]. Int J Biochem Cell Biol, 2008, 40(10):2129-2140.
[48]
Heukels P, Van Hulst J, Van Nimwegen M, et al. Fibrocytes are increased in lung and peripheral blood of patients with idiopathic pulmonary fibrosis[J]. Respir Res, 2018, 19(1):90.
[49]
Margaritopoulos GA, Giannarakis I, Siafakas N. An update on idiopathic pulmonary fibrosis[J]. Panminerva Med, 2013, 55(2):109-120.
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