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本文引用的文献

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Mechanisms for the Resolution of Organ Fibrosis.器官纤维化的解决机制。
Physiology (Bethesda). 2019 Jan 1;34(1):43-55. doi: 10.1152/physiol.00033.2018.
2
The matricellular protein CCN1 in tissue injury repair.组织损伤修复中的基质细胞蛋白CCN1
J Cell Commun Signal. 2018 Mar;12(1):273-279. doi: 10.1007/s12079-018-0450-x. Epub 2018 Jan 22.
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Cellular senescence mediates fibrotic pulmonary disease.细胞衰老介导肺纤维化疾病。
Nat Commun. 2017 Feb 23;8:14532. doi: 10.1038/ncomms14532.
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The matricellular protein CCN1 enhances TGF-β1/SMAD3-dependent profibrotic signaling in fibroblasts and contributes to fibrogenic responses to lung injury.基质细胞蛋白CCN1增强成纤维细胞中TGF-β1/SMAD3依赖性促纤维化信号传导,并促进对肺损伤的纤维化反应。
FASEB J. 2016 Jun;30(6):2135-50. doi: 10.1096/fj.201500173. Epub 2016 Feb 16.
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Blue journal conference. Aging and susceptibility to lung disease.蓝色期刊会议。衰老与肺部疾病易感性。
Am J Respir Crit Care Med. 2015 Feb 1;191(3):261-9. doi: 10.1164/rccm.201410-1876PP.
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Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance.靶向 Nox4-Nrf2 氧化还原失衡逆转衰老相关持续性纤维化。
Sci Transl Med. 2014 Apr 9;6(231):231ra47. doi: 10.1126/scitranslmed.3008182.
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Aging increases CCN1 expression leading to muscle senescence.衰老会导致 CCN1 表达增加,从而导致肌肉衰老。
Am J Physiol Cell Physiol. 2014 Jan 1;306(1):C28-36. doi: 10.1152/ajpcell.00066.2013. Epub 2013 Nov 6.
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Mechanistic links between aging and lung fibrosis.衰老与肺纤维化之间的机制联系。
Biogerontology. 2013 Dec;14(6):609-15. doi: 10.1007/s10522-013-9451-6. Epub 2013 Aug 9.
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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)
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Cellular senescence controls fibrosis in wound healing.细胞衰老控制伤口愈合中的纤维化。
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特发性肺纤维化患者血浆中的衰老相关细胞基质蛋白 CCN1。

The senescence-associated matricellular protein CCN1 in plasma of human subjects with idiopathic pulmonary fibrosis.

机构信息

Division of Pulmonary, Allergy, Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

Division of Pulmonary, Allergy, Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

出版信息

Respir Med. 2020 Jan;161:105821. doi: 10.1016/j.rmed.2019.105821. Epub 2019 Nov 19.

DOI:10.1016/j.rmed.2019.105821
PMID:31765873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7023981/
Abstract

INTRODUCTION

Cellular senescence has been linked to the pathogenesis of idiopathic pulmonary fibrosis (IPF). CCN1 is a matricellular protein that has been shown to induce cellular senescence and contribute to lung fibrosis in pre-clinical models. In this report, we determined plasma CCN1 levels in patients with IPF and its potential role in clinical outcomes.

METHODS AND RESULTS

We evaluated 88 patients diagnosed with IPF at the University of Alabama at Birmingham. CCN1 levels were measured in plasma specimens by ELISA. The primary outcome measure was transplant-free survival (TFS) duration. High-CCN1 levels were associated with a lower transplant-free survival independent of %FVC and %DCO compared to patients with low plasma CCN1 (HR = 2.15; 95%CI 1.04-4.45, p = 0.04).

CONCLUSION

This study demonstrates that plasma levels of CCN1 may be predictive of survival in IPF. Given the plausible role of CCN1 in cellular senescence and pathobiology of IPF, the predictive value of CCN1 in disease progression among patients with IPF warrants further investigation.

摘要

简介

细胞衰老与特发性肺纤维化(IPF)的发病机制有关。CCN1 是一种基质细胞蛋白,已被证明可诱导细胞衰老,并在临床前模型中导致肺纤维化。在本报告中,我们测定了 IPF 患者的血浆 CCN1 水平及其在临床结局中的潜在作用。

方法和结果

我们在阿拉巴马大学伯明翰分校评估了 88 例诊断为 IPF 的患者。通过 ELISA 法测定血浆标本中的 CCN1 水平。主要观察指标是无移植存活率(TFS)持续时间。与低血浆 CCN1 相比,高 CCN1 水平与较低的 TFS 独立于 %FVC 和 %DCO 相关(HR=2.15;95%CI 1.04-4.45,p=0.04)。

结论

本研究表明,血浆 CCN1 水平可能可预测 IPF 的生存情况。鉴于 CCN1 在细胞衰老和 IPF 病理生物学中的潜在作用,CCN1 在 IPF 患者疾病进展中的预测价值值得进一步研究。