期刊文献+

胸膜间皮细胞在肺纤维化中的作用及机制研究进展

Research Progress in Role and Mechanism of Pleural Mesothelial Cells in Pulmonary Fibrosis
下载PDF
导出
摘要 肺纤维化是多种原因引起肺脏损伤时,肺自身过度抗损伤修复的结果,其是源于肺泡上皮细胞的慢性炎症损伤。近年来随着研究的深入,发现胸膜间皮细胞(PMCs)特殊的细胞结构及多样的生物学作用在肺纤维化的发生发展中有重要作用;炎症刺激后PMCs可发生上皮-间充质转化,其细胞表型发生改变,同时细胞迁移能力增强,从胸膜腔向胸膜下肺内组织迁移,导致胸膜下纤维化的形成,是纤维化组织成纤维细胞和细胞外基质的重要来源之一。多种信号通路、表观遗传学及细胞的免疫调节作用参与并调控PMCs损伤引起肺纤维化的过程,且各种信号之间可能存在某些关联,进一步促进了肺纤维化的发生发展,因此对PMCs的研究有望为肺纤维化的治疗提供新方向。 Pulmonary fibrosis is the result of excessive anti-injury repair of the lung itself when lung is injured by a variety of causes,which is chronic inflammatory injury originating from alveolar epithelial cells.In recent years,with the deepening of research,it′s discovered that the special cellular structure and diverse biological roles of pleural mesothelial cells(PMCs)play an important role in the occurrence and development of pulmonary fibrosis.PMCs can undergo epithelial-mesenchymal transition after inflammatory stimulation,and their cell phenotype changes,while the cell migration ability is enhanced,migrating from the pleural cavity to the subpleural lung tissue,leading to the formation of subpleural fibrosis,which is one of the important sources of fibroblasts and extracellular matrix in fibrotic tissue.A variety of signaling pathways,epigenetics,and cellular immunoregulation are involved in and regulate the process of pulmonary fibrosis caused by PMCs injury,and there may be some associations between various signals that further promote the occurrence and development of pulmonary fibrosis,so the study of PMCs is expected to provide a new direction for the treatment of pulmonary fibrosis.
作者 马喜田 陈利军 万毅新 MA Xitian;CHEN Lijun;WAN Yixin(Department of Respiratory Medicine,Lanzhou University Second Hospital,Lanzhou 730030,China;The Second Clinical Medical College of Lanzhou University,Lanzhou 730030,China)
出处 《医学综述》 CAS 2023年第8期1502-1509,共8页 Medical Recapitulate
基金 兰州大学第二医院“萃英科技创新”计划项目(2020QN-23) 甘肃省高等学校创新基金项目(2021B-028)。
关键词 肺纤维化 胸膜间皮细胞 上皮-间充质转化 免疫调节 Pulmonary fibrosis Pleural mesothelial cells Epithelial-mesenchymal transition Immunoregulation
  • 相关文献

参考文献5

二级参考文献23

  • 1Matthias Ocker.Deacetylase inhibitors-focus on non-histone targets and effects[J].World Journal of Biological Chemistry,2010,1(5):55-61. 被引量:11
  • 2Manley GT, Fujimura M, Ma T, et al. Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke. Nat Med, 2000,6 : 159-163. 被引量:1
  • 3Cuzzocrea S, Mazzon E, Calabro G, et al. Inducible nitric oxide synthase-knockout mice exhibit resistance to pleurisy and lung injury caused by carrageenan. Am J Respir Crit Care Med, 2000, 162 : 1859-1866. 被引量:1
  • 4Sakaguchi Y, Shirahase H, Kunishiro K, et al. Effect of combination of nitric oxide synthase and cyclooxygenase inhibitors on carrageenan-induced pleurisy in rats. Life Sci, 2006,79 : 442- 447. 被引量:1
  • 5Agre P. The aquaporin water channels. Proc Am Thorac Soc, 2006,3:5-13. 被引量:1
  • 6Bai C, Fukuda N, Song Y, et al. Lung fluid transport in aquaporin-1 and aquaporin4 knockout mice. J Clin Invest, 1999, 103:555-561. 被引量:1
  • 7Antony VB. Immunological mechanisms in pleural disease. Eur Respir J, 2003,21:539-544 被引量:1
  • 8Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCRand the 2 (-Delta Deita C(T) ) Method D].Methods, 2001,25(4 ):402-408. 被引量:1
  • 9Drent M,Cobben NA,Henderson RF,et al.Usefulness of lactate dehy?drogenase and its isoenzymes as indicators of lung damage or inflam?mation[J].Eur Respir,1996, 9(8):1736-1742. 被引量:1
  • 10Discoll KE, MaurerJK, Lindenschmidt RC, et al. Respiratory track response to dust: relationships between dust hurden lung injury, alveolar macrophage fibnectin release, and the development of pulmonary fibrosisDJ. Toxicol Appl Pharmacol, 1990, 106 ( 1): 88- 101. 被引量:1

共引文献17

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部