特发性肺纤维化中的信号转导通路

doi:10.3969/j.issn.1674-490X.2009.02.035

医学研究与教育 ›› 2009, Vol. 26 ›› Issue (2): 79-81,98.DOI: 10.3969/j.issn.1674-490X.2009.02.035

特发性肺纤维化中的信号转导通路

祖金池¹,崔娜²,段斐²

1.河北大学附属医院,胸外科,河北,保定,071000
2.河北大学基础医学教研中心,河北,保定,071000

收稿日期:2016-10-09 修回日期:2016-10-09 出版日期:2009-04-25 发布日期:2009-04-25

Received:2016-10-09 Revised:2016-10-09 Online:2009-04-25 Published:2009-04-25

摘要/Abstract

摘要： 特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)是一种病因不明,发病机制不清,缺乏治疗手段的致命性漫性肺间质疾病,其病理特征是肺泡上皮损伤,成纤维细胞灶(fibroblast foci)的形成以及细胞外基质(Extracellula matrix,ECM)的过度沉积,最终导致了肺组织结构的异常重塑.

中图分类号:

R563

祖金池,崔娜,段斐. 特发性肺纤维化中的信号转导通路[J]. 医学研究与教育, 2009, 26(2): 79-81,98.

[1] Thannickal VJ, Horowitz JC. [J]. Proceedings of the American Thoracic Society 2006.
[2] Horowitz J, Thannickal V. Idiopathic Pulmonary Fibrosis:new concepts in pathogenesis and implications for drug therapy [J]. Treatments in Respiratory Medicine 2006, 5(05).
[3] Selman M, Pardo A, Kaminski N. Idiopathic Pulmonary Fibrosis:Aberrant Recapitulation of Developmental Programs? [J]. PLOS MEDICINE 2008, 5(03).
[4] Shimizu, Y, Dobashi, K, Iizuka, K, Horie, T, Suzuki, K, Tukagoshi, H, Nakazawa, T, Nakazato, Y, Mori, M. Contribution of small GTPase Rho and its target protein rock in a murine model of lung fibrosis. [J]. American journal of respiratory and critical care medicine 2001, 1(1).
[5] Watts K, Cottrell E, Hoban P. RhoA signaling modulates cyclin D1 expression in human lung fibroblasts;im plications for idiopathic pulmonary fibrosis [J]. Respiratory Research 2006, 7(01).
[6] Konigshoff M. Functional Wnt Signaling Is Increased in Idiopathic Pulmonary Fibrosis [J]. PloS ONE 2008, 3(05).
[7] Chilosi M, Poletti V, Zamò A. Aberrant Wnt/β-Catenin Pathway Activation in Idiopathic Pulmonary Fibrosis [J]. American Journal of Pathology 2003, 162(05).
[8] Morrisey E. Wnt Signaling and Pulmonary Fibrosis [J]. American Journal of Pathology 2003, 162(05).
[9] Hardie W, Korfhagen T, Sartor M. Genomic Profile of Matrix and Vasculature Remodeling in TGF-α Induced Pul monary Fibrosis [J]. American Journal of Respiratory Cell and Molecular Biology 2007, 37(03).
[10] Allen J, Spiteri M. Growth factors in idiopathic pulmonary fibrosis:relative roles [J]. Respiratory Research 2002, 3(01).
[11] Willis B, Liebler J, Luby-Phelps K. Induction of Epithelial-Mesenchymal Transition in Alveolar Epithelial Ceils by Transforming Growth Factor-β1 Potential Role in Idiopathic Pulmonary Fibrosis [J]. American Journal of Pathology 2005, 166(05).
[12] Willis B, Borok Z. TGF-β-induced EMT:mechanisms and implications for fibrotic lung disease [J]. American Journal of Physiology-Lung Cellular and Molecular Physiology 2007, 293(03).
[13] Wang XM, Zhang Y, Kim HP, Zhou Z, Feghali-Bostwick CA, Liu F, Ifedigbo E, Xu X, Oury TD, Kaminski N, Choi AM. Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. [J]. The Journal of Experimental Medicine 2006, 13(13).
[14] Allen J, Knisht R, Bloor C. Enhanced Insulin-Like Growth Factor Binding Protein-Related Protein 2(Connective Tissue Growth Factor)Expression in Patients with Idiopathic Pulmonary Fibrosis and Pulmonary Sarcoidosis [J]. American Journal of Respiratory Cell and Molecular Biology 1999, 21(06).
[15] Pan L-H, Yamauchi K, Uzuki M. Type Ⅱ alveolar epithelial cells and interstitial fibmblasts express connective tissue growth factor in IPF [J]. European Respiratory Journal 2001, 17(06).
[16] Agostini C, Gurrieri C. Chemokine/cytokine cocktail in idiopathic pulmonary fibrosis. [J]. Proceedings of the American Thoracic Society 2006, 4(4).
[17] Daian T, Ohtsuru A, Rogounovitch T, Ishihara H, Hirano A, Akiyama Uchida Y, Saenko V, Fujii T, Yamashita S. [J]. The Journal of Investigative Dermatology 2003.
[18] Kuwano K, Hagimoto N, Kawasaki M, Yatomi T, Nakamura N, Nagata S, Suda T, Kunitake R, Maeyama T, Miyazaki H, Hara N. [J]. The Journal of Clinical Investigation: The Official Journal of the American Society for Clinical Investigation 1999.
[19] Miyazaki H, Kuwano K, Yoshida K. The pefforin mediated apoptotic pathway in lung injury and fibrosis [J]. Journal of Clinical Pathology 2004, 57(12).
[20] DosReis G, Borges V. Role of Fas-Ligand Induced Apoptosis in Puimonary Inflammation and Injury [J]. Current Drug Targets-Inflammation and Allergy 2003, 2(02).
[21] Nakashima N, Kuwano K, Maeyama T. The p53 Mdm2 association in epithelial cells in idiopathic pulmonary fibrosis and non-specific interstitial pneumonia [J]. Journal of Clinical Pathology 2005, 58(06).
[22] Koli K, Myllgrniemi M, Vuorinen K. Bone Morphogenetic Protein-4 Inhibitor Gremlin Is Overexpressed in Idiopathic Pulmonary Fibrosis [J]. American Journal of Pathology 2006, 169(01).
[23] Martin M, Buckenberger J, Jiang J. TGF-β1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and P13K signaling pathways [J]. American Journal of Physiology-Lung Cellular and Molecular Physiology 2007, 293(03).

特发性肺纤维化中的信号转导通路

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