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The potential role of PDGF, IGF-1, TGF-beta expression in idiopathic pulmonary fibrosis.血小板衍生生长因子、胰岛素样生长因子-1、转化生长因子-β表达在特发性肺纤维化中的潜在作用。
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本文引用的文献

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Challenges in IPF diagnosis, current management and future perspectives: Patient case 2.
Sarcoidosis Vasc Diffuse Lung Dis. 2015 Aug 3;32 Suppl 1:38-9.
2
[The expressions and meanings of BMP-7 and TGF-β in idiopathic pulmonary fibrosis and idiopathic nonspecific interstitial pneumonia].[骨形态发生蛋白-7和转化生长因子-β在特发性肺纤维化和特发性非特异性间质性肺炎中的表达及意义]
Zhonghua Jie He He Hu Xi Za Zhi. 2014 Sep;37(9):664-70.
3
An official American Thoracic Society/European Respiratory Society statement: Update of the international multidisciplinary classification of the idiopathic interstitial pneumonias.美国胸科学会/欧洲呼吸学会官方声明:特发性间质性肺炎的国际多学科分类的更新。
Am J Respir Crit Care Med. 2013 Sep 15;188(6):733-48. doi: 10.1164/rccm.201308-1483ST.
4
Kindlin-2 mediates activation of TGF-β/Smad signaling and renal fibrosis.Kindlin-2 介导 TGF-β/Smad 信号通路的激活和肾脏纤维化。
J Am Soc Nephrol. 2013 Sep;24(9):1387-98. doi: 10.1681/ASN.2012101041. Epub 2013 May 30.
5
The pathogenesis of cardiac fibrosis.心脏纤维化的发病机制。
Cell Mol Life Sci. 2014 Feb;71(4):549-74. doi: 10.1007/s00018-013-1349-6. Epub 2013 May 7.
6
Usual interstitial pneumonia coexisted with nonspecific interstitial pneumonia, What's the diagnosis?常同时存在于非特异性间质性肺炎,这是什么诊断?
Diagn Pathol. 2012 Dec 3;7:167. doi: 10.1186/1746-1596-7-167.
7
Targeting the TGFβ signalling pathway in disease.靶向疾病中的 TGFβ 信号通路。
Nat Rev Drug Discov. 2012 Oct;11(10):790-811. doi: 10.1038/nrd3810. Epub 2012 Sep 24.
8
An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management.特发性肺纤维化:诊断和管理的循证指南(美国胸科学会/欧洲呼吸学会/日本呼吸学会/拉丁美洲胸科学会联合发布)
Am J Respir Crit Care Med. 2011 Mar 15;183(6):788-824. doi: 10.1164/rccm.2009-040GL.
9
TGF-beta driven lung fibrosis is macrophage dependent and blocked by Serum amyloid P.TGF-β 驱动的肺纤维化依赖于巨噬细胞,并被血清淀粉样蛋白 P 阻断。
Int J Biochem Cell Biol. 2011 Jan;43(1):154-62. doi: 10.1016/j.biocel.2010.10.013. Epub 2010 Oct 29.
10
[A study on the efficacy of glucocorticoid therapy for idiopathic nonspecific interstitial pneumonia].[糖皮质激素治疗特发性非特异性间质性肺炎的疗效研究]
Zhonghua Jie He He Hu Xi Za Zhi. 2010 Aug;33(8):593-6.

血小板衍生生长因子的低表达与特发性非特异性间质性肺炎患者更好的总生存率相关。

Lower expression of platelet derived growth factor is associated with better overall survival rate of patients with idiopathic nonspecific interstitial pneumonia.

作者信息

Zhu Xuyou, Fang Xia, Chen Wei, Han Fei, Huang Ziling, Luo Benfang, Gu Pan, Zhang Long, Qiu Weizhe, Zeng Yu, Rui Weiwei, Yi Xianghua

机构信息

Department of Pathology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.

Department of Hematology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.

出版信息

J Thorac Dis. 2017 Mar;9(3):519-528. doi: 10.21037/jtd.2017.02.50.

DOI:10.21037/jtd.2017.02.50
PMID:28449458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5394091/
Abstract

BACKGROUND

Idiopathic nonspecific interstitial pneumonia (INSIP) presents with varying degrees of interstitial inflammation and fibrosis exhibiting a uniform appearance. Lack of knowledge on the underlying mechanisms of INSIP has contributed to few effective treatment strategies. Our study is designed to explore aberrantly expressed cytokines involvement in INSIP development.

METHODS

Oligo GEArray was employed to detect the expression of cytokines in INSIP patients, and idiopathic pulmonary fibrosis (IPF) was setup as isotype control. Real-time PCR and immunohistochemistry analysis were used to further confirm the expression of abnormally expressed cytokines. The correlationship between cytokines expression and overall survival rate of patients with IPF and INSIP were analyzed.

RESULTS

From microarray detection, transforming growth factor-beta-1 (TGF-β1), fibroblast growth factor 10 (FGF10), and platelet derived growth factor (PDGF) were predominantly up-regulated in patients with INSIP. Real-time PCR and immunohistochemistry also showed these cytokines was abnormally expressed in INSIP. In addition to, the clinical relevance analysis demonstrated relatively lower expression of PDGF patients had longer overall survival rate than those with higher expression of PDGF.

CONCLUSIONS

Our study suggests that TGF-β1, FGF10, and PDGF are required for the pathogenesis of INSIP, and may therefore be ideal targets in INSIP treatment. Moreover, INSIP patients with lower expression of PDGF had better survival rate.

摘要

背景

特发性非特异性间质性肺炎(INSIP)表现为不同程度的间质性炎症和纤维化,呈现出一致的外观。对INSIP潜在机制的认识不足导致有效的治疗策略较少。我们的研究旨在探讨异常表达的细胞因子在INSIP发病机制中的作用。

方法

采用寡核苷酸基因芯片检测INSIP患者细胞因子的表达,并将特发性肺纤维化(IPF)作为同型对照。采用实时荧光定量PCR和免疫组织化学分析进一步证实异常表达细胞因子的表达。分析细胞因子表达与IPF和INSIP患者总生存率的相关性。

结果

通过基因芯片检测,转化生长因子-β1(TGF-β1)、成纤维细胞生长因子10(FGF10)和血小板衍生生长因子(PDGF)在INSIP患者中主要上调。实时荧光定量PCR和免疫组织化学也显示这些细胞因子在INSIP中异常表达。此外,临床相关性分析表明,PDGF表达相对较低的患者总生存率高于PDGF表达较高的患者。

结论

我们的研究表明,TGF-β1、FGF10和PDGF是INSIP发病机制所必需的,因此可能是INSIP治疗的理想靶点。此外,PDGF表达较低的INSIP患者生存率更高。