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β2-microglobulin as a biomarker of pulmonary fibrosis development in COPD patients

机译:β2-微球蛋白作为COPD患者肺纤维化发育的生物标志物

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摘要

Expression of β2-microglobulin (β2M) is involved in fibrosis progression in kidney, liver, and heart. In this case-controlled retrospective study, we investigated the role of β2M in the development of pulmonary fibrosis in patients with chronic obstructive pulmonary disease (COPD). Analysis of 450 COPD patients revealed that patients with decreased pulmonary diffusing capacity (DLCO) had increased β2M serum levels. Compared to patients with lower β2M serum levels, patients with increased β2M levels exhibited increased alveolar wall/septal thickening and lung tissue β2M expression. In addition, patients with increased β2M levels had increased lung expression of TGF-β1, Smad4, and a-SMA. Animal experiments showed that increased β2M expression resulted in epithelial-mesenchymal transition (EMT), alveolar wall/septal thickening, and pulmonary fibrosis in a rat COPD model. Together, these results indicate that β2M serum levels may serve as a new indicator for assessment of pulmonary diffusion function and pulmonary fibrosis severity in clinical practice and may provide a potential target for treatment of pulmonary fibrosis in the future.
机译:β2-微球蛋白(β2M)的表达参与肾脏,肝脏和心脏纤维化进展。在这种案例控制的回顾性研究中,我们研究了β2M在慢性阻塞性肺病(COPD)患者肺纤维化发育中的作用。对450名COPD患者的分析表明,肺部扩散能力下降(DLCO)的患者增加了β2M血清水平。与β2M血清水平较低的患者相比,β2M水平增加的患者表现出肺泡壁/隔膜增厚和肺组织β2M表达增加。此外,β2M水平升高的患者具有增加的TGF-β1,SMAD4和SMA的肺部表达。动物实验表明,β2M表达增加导致上皮 - 间充质转换(EMT),肺泡壁/隔膜增厚,以及大鼠COPD模型中的肺纤维化。这些结果表明,β2M血清水平可以用作评估临床实践中肺部扩散函数和肺纤维化严重程度的新指标,并且可以为未来治疗肺纤维化的潜在靶标。

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