期刊文献+

谷氨酰胺代谢在肺纤维化疾病中的研究进展 被引量:1

Research progress on glutamine metabolism in pulmonary fibrosis
下载PDF
导出
摘要 肺纤维化是一种进展迅速的肺部疾病,以成纤维细胞增殖及大量细胞外基质沉积、肺组织结构破坏为特征的间质性肺疾病。其中位生存期为3-4年。目前治疗方法有限,预后较差。最近在器官纤维化中发现了多种代谢异常,其中包括谷氨酰胺代谢异常。文章主要就谷氨酰胺代谢过程在促进肺纤维化发病过程中的作用研究进展进行综述。 Pulmonary fibrosis is a rapidly progressive lung disease characterized by fibroblast proliferation,massive extracellular matrix deposition and destruction of lung tissue,with limited treatments and poor prognosis.Its median survival was 3 to 4 years.A variety of metabolic abnormalities,such as glutamine metabolism abnormalities,have recently been identified in organ fibrosis.This review discusses how glutamine metabolic processes promote the pathogenesis of pulmonary fibrosis.
作者 殷娥高 杨眉(综述) 雷雯 董昭兴(审校) YIN E-gao;YANG Mei;LEI Wen;DONG Zhao-xing(Respiratory and Critical Illness Ward 1,the Second Affiliated Hospital of Kunming Medical University,Kunming 650101,Yunnan,China;Respiratory Department of Ningbo Huamei Hospital,University of Chinese Academy of Sciences,Ningbo 315000,Zhejiang,China)
出处 《医学研究生学报》 CAS 北大核心 2021年第12期1331-1334,共4页 Journal of Medical Postgraduates
基金 昆明医科大学研究生创新基金(2021S201)。
关键词 肺纤维化 谷氨酰胺代谢 谷氨酰胺酶 pulmonary fibrosis glutamine metabolism glutaminase
  • 相关文献

参考文献2

二级参考文献47

  • 1Hinz B,Gabbiani G.Fibrosis:recent advances in myofibroblast biology and new therapeutic perspectives[J].Biol Rep,2010,2: 78.
  • 2Matsuzawa Y,Kawashima T,Yamazaki R,et al.Inhibitory effects of clinical reagents having anti-oxidative activity on transforming growth factor-β1-induced expression of α-smooth muscle actin in human fetal lung fibroblasts[J].J Toxicol Sci,2011,36(6): 733-740.
  • 3Uhal BD,Ramos C,Joshi I,et al.Cell size,cell cycle,and alpha-smooth muscle actin expression by primary human lung fibroblasts[J].Am J Physiol,1998,275(5 Pt 1): L998-L1005.
  • 4Peng H,Carretero OA,Peterson EL,et al.Ac-SDKP inhibits transforming growth factor-beta1-induced differentiation of human cardiac fibroblasts into myofibroblasts[J].Am J Physiol Heart Circ Physiol,2010,298(5): H1357-H1364.
  • 5Conte E,Fruciano M,Fagone E,et al.Inhibition of PI3K prevents the proliferation and differentiation of human lung fibroblasts into myofibroblasts: the role of class I P110 isoforms[J].PLoS One,2011,6(10): e24663.
  • 6Geng J, Huang X, Li Y, et al. Phosphatase and tensin homolog deleted on chromosome 10 contributes to phenotype transformation of fibroblasts in idiopathic pulmonary fibrosis via multiple pathways[J]. Exp Biol Med (Maywood), 2016,241(2):157-165.
  • 7Bagnato G, Harari S. Cellular interactions in the pathogenesis of interstitial lung diseases[J]. Eur Respir Rev, 2015, 24(135): 102-114.
  • 8Wuyts WA, Agostini C, Antoniou KM, et al. The pathogenesis of pulmonary fibrosis: a moving target[J]. Eur Respir J, 2013, 41(5): 1207-1218.
  • 9Mccubbrey AL, Curtis JL. Efferocytosis and lung disease[J]. Chest, 2013, 143(6): 1750-1757.
  • 10Cai M, Bonella F, He X, et al. CCL18 in serum, BAL fluid and alveolar macrophage culture supernatant in interstitial lung diseases[J]. Respir Med, 2013, 107(9): 1444-1452.

共引文献28

同被引文献6

引证文献1

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