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本文引用的文献

1
Activation of calpain by renin-angiotensin system in pleural mesothelial cells mediates tuberculous pleural fibrosis.肾素-血管紧张素系统激活胸膜间皮细胞中的钙蛋白酶可介导结核性胸膜纤维化。
Am J Physiol Lung Cell Mol Physiol. 2016 Jul 1;311(1):L145-53. doi: 10.1152/ajplung.00348.2015. Epub 2016 Jun 3.
2
Mycobacterium tuberculosis Upregulates TNF-α Expression via TLR2/ERK Signaling and Induces MMP-1 and MMP-9 Production in Human Pleural Mesothelial Cells.结核分枝杆菌通过TLR2/ERK信号上调TNF-α表达并诱导人胸膜间皮细胞产生MMP-1和MMP-9。
PLoS One. 2015 Sep 14;10(9):e0137979. doi: 10.1371/journal.pone.0137979. eCollection 2015.
3
Spectrin Breakdown Products (SBDPs) as Potential Biomarkers for Neurodegenerative Diseases.血影蛋白降解产物(SBDPs)作为神经退行性疾病的潜在生物标志物
Curr Transl Geriatr Exp Gerontol Rep. 2012 Jun;1(2):85-93. doi: 10.1007/s13670-012-0009-2.
4
Angiotensin-converting enzyme (ACE) gene polymorphisms are associated with idiopathic pulmonary fibrosis.血管紧张素转化酶(ACE)基因多态性与特发性肺纤维化有关。
Lung. 2013 Aug;191(4):345-51. doi: 10.1007/s00408-013-9469-1. Epub 2013 May 9.
5
ACE/ACE2 ratio and MMP-9 activity as potential biomarkers in tuberculous pleural effusions.ACE/ACE2 比值和 MMP-9 活性作为结核性胸腔积液的潜在生物标志物。
Int J Biol Sci. 2012;8(8):1197-205. doi: 10.7150/ijbs.5087. Epub 2012 Oct 17.
6
Calpain-1 regulation of matrix metalloproteinase 2 activity in vascular smooth muscle cells facilitates age-associated aortic wall calcification and fibrosis.钙蛋白酶-1 调节血管平滑肌细胞基质金属蛋白酶 2 的活性,促进与年龄相关的主动脉壁钙化和纤维化。
Hypertension. 2012 Nov;60(5):1192-9. doi: 10.1161/HYPERTENSIONAHA.112.196840. Epub 2012 Sep 24.
7
Nebivolol reduces cardiac angiotensin II, associated oxidative stress and fibrosis but not arterial pressure in salt-loaded spontaneously hypertensive rats.比索洛尔可降低盐负荷自发性高血压大鼠心脏血管紧张素 II、氧化应激和纤维化,但不降低动脉压。
J Hypertens. 2012 Sep;30(9):1766-74. doi: 10.1097/HJH.0b013e328356766f.
8
Comparison of localized versus systemic levels of Matrix metalloproteinases (MMPs), its tissue inhibitors (TIMPs) and cytokines in tuberculous and non-tuberculous pleuritis patients.比较结核性和非结核性胸膜炎患者局部与全身基质金属蛋白酶(MMPs)及其组织抑制剂(TIMPs)和细胞因子水平。
Hum Immunol. 2012 Oct;73(10):985-91. doi: 10.1016/j.humimm.2012.07.042. Epub 2012 Jul 20.
9
Calpain mediates pulmonary vascular remodeling in rodent models of pulmonary hypertension, and its inhibition attenuates pathologic features of disease.钙蛋白酶在肺动脉高压的啮齿动物模型中介导肺血管重构,其抑制可减轻疾病的病理特征。
J Clin Invest. 2011 Nov;121(11):4548-66. doi: 10.1172/JCI57734. Epub 2011 Oct 17.
10
The calpain inhibitor calpeptin prevents bleomycin-induced pulmonary fibrosis in mice.钙蛋白酶抑制剂 calpeptin 可预防博来霉素诱导的小鼠肺纤维化。
Clin Exp Immunol. 2010 Dec;162(3):560-7. doi: 10.1111/j.1365-2249.2010.04257.x. Epub 2010 Sep 15.

钙蛋白酶和血影蛋白降解产物作为结核性胸腔积液的潜在生物标志物

Calpain and spectrin breakdown products as potential biomarkers in tuberculous pleural effusion.

作者信息

Hong Ji Young, Park So Yeong, Kim Youngmi, Lee Chang Youl, Lee Myung Goo

机构信息

Division of Pulmonary, Allergy and Critical Care Medicine, Department of Internal Medicine, Chuncheon Sacred Heart Hospital, Hallym University Medical Center, Chuncheon, Gangwon-do, Republic of Korea.

Lung Research Institute, Hallym University College of Medicine, Chuncheon, Gangwon-do, Republic of Korea.

出版信息

J Thorac Dis. 2018 May;10(5):2558-2566. doi: 10.21037/jtd.2018.04.85.

DOI:10.21037/jtd.2018.04.85
PMID:29997916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6006058/
Abstract

BACKGROUND

Early diagnosis of tuberculous pleural effusion (TPE) remains difficult. Calpain is a family of calcium-dependent endopeptidase that plays an important role in extracellular matrix (ECM) remodeling and collagen synthesis. The aim of this study was to explore the diagnostic value of pleural fluid angiotensin-converting enzyme (ACE), calpain-1, spectrin breakdown products (SBDP), and matrix metalloproteinase-1 (MMP-1) in TPE and malignant pleural effusion (MPE).

METHODS

The study included 47 patients with TPE, 28 patients with MPE, and 10 patients with transudate of non-tuberculous and non-malignant origin as controls. Calpain-1, ACE, SBDP, and MMP-1 levels in pleural fluid were measured by the ELISA method.

RESULTS

ACE, calpain-1, SBDP, and MMP-1 levels were higher in TPE than MPE and transudate (all, P<0.05). On multivariate logistic regression analysis, adenosine deaminase (ADA) ≥40 IU/mL, calpain-1 ≥787 ng/mL, and SBDP ≥2.745 ng/mL were independent factors associated with TPE. The predicted probability of TPE based on these three predictors had an area under the receiver operating characteristic (ROC) curve of 0.985, with 97.9% sensitivity and 86.6% specificity under a cut-off value of 0.326. In patients with TPE, residual pulmonary thickening (RPT) was associated with significantly higher calpain-1, SBDP, and MMP-1 levels (all, P<0.05) versus cases without RPT.

CONCLUSIONS

Our results suggest that the overproduction of calpain-1 and SBDP is associated with pleural fibrosis in tuberculous pleurisy. While ADA is a conventional marker for diagnostic TPE, the simultaneous measurement of calpain-1 and SBDP l in pleural fluid may improve the diagnostic efficacy.

摘要

背景

结核性胸腔积液(TPE)的早期诊断仍然困难。钙蛋白酶是一类钙依赖性内肽酶,在细胞外基质(ECM)重塑和胶原蛋白合成中起重要作用。本研究旨在探讨胸腔积液血管紧张素转换酶(ACE)、钙蛋白酶-1、血影蛋白降解产物(SBDP)和基质金属蛋白酶-1(MMP-1)在TPE和恶性胸腔积液(MPE)中的诊断价值。

方法

本研究纳入47例TPE患者、28例MPE患者以及10例非结核非恶性来源的漏出液患者作为对照。采用酶联免疫吸附测定(ELISA)法检测胸腔积液中钙蛋白酶-1、ACE、SBDP和MMP-1水平。

结果

TPE患者胸腔积液中ACE、钙蛋白酶-1、SBDP和MMP-1水平高于MPE患者和漏出液患者(均P<0.05)。多因素逻辑回归分析显示,腺苷脱氨酶(ADA)≥40 IU/mL、钙蛋白酶-1≥787 ng/mL和SBDP≥2.745 ng/mL是与TPE相关的独立因素。基于这三个预测指标的TPE预测概率在受试者工作特征(ROC)曲线下的面积为0.985,在截断值为0.326时,敏感性为97.9%,特异性为86.6%。在TPE患者中,与无残留肺增厚(RPT)的病例相比,有RPT的患者钙蛋白酶-1、SBDP和MMP-1水平显著更高(均P<0.05)。

结论

我们的结果表明,钙蛋白酶-1和SBDP的过度产生与结核性胸膜炎中的胸膜纤维化有关。虽然ADA是诊断TPE的传统标志物,但同时检测胸腔积液中的钙蛋白酶-1和SBDP可能会提高诊断效能。