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COPD 中 HIF1-A 表达与气道重塑的相关性。

Correlation Between HIF1-A Expression and Airway Remodeling in COPD.

机构信息

The Nanhua Affiliated Hospital, Department of Respiratory Physicians, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, People's Republic of China.

The Nanhua Affiliated Hospital, Department of General Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, People's Republic of China.

出版信息

Int J Chron Obstruct Pulmon Dis. 2024 Apr 13;19:921-931. doi: 10.2147/COPD.S447256. eCollection 2024.

DOI:10.2147/COPD.S447256
PMID:38633565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11022883/
Abstract

BACKGROUND

Airway remodeling is a significant pathological characteristic of chronic obstructive pulmonary disease (COPD). In recent years, hypoxia-inducible factor 1-α (HIF-1α), a member of the hypoxia-inducible factor protein family, has gained attention. However, the potential correlation between HIF-1α and COPD airway remodeling remains unclear.

OBJECTIVE

This study explored the expression patterns of HIF-1α in patients with COPD and its association with airway remodelling. This investigation aims to furnish novel insights for the clinical identification of prospective therapeutic targets for ameliorating COPD-related airway remodelling.

PATIENTS AND METHODS

A total of 88 subjects were included, consisting of 28 controls and 60 COPD patients. Various staining methods were employed to observe the pathological changes in airway tissues. Immunohistochemistry was utilized to detect the expression of HIF-1α and MMP9 (matrix metalloproteinase 9) in airway tissues. Enzyme-linked immunosorbent assay (ELISA) was used to measure the concentration in serum of HIF-1α and MMP9. Computed tomography (CT) airway parameters were measured in all participants to assess airway remodeling. The relationship between serum HIF-1α and MMP9 concentrations and airway parameters was analyzed.

RESULTS

Staining of airway structures in COPD patients revealed significant pathological changes associated with airway remodelling, including mixed cilia and subepithelial fibrosis. The expression of HIF-1α and MMP9 was significantly higher in both human airway tissue and serum compared to controls. Chest CT scans exhibited typical imaging features of airway remodeling and increased airway parameters.

CONCLUSION

The findings suggest a correlation between increased HIF-1α expression and COPD airway remodelling. This study provides novel evidence that HIF-1α may be a potential biomarker for airway remodelling in COPD patients.

摘要

背景

气道重塑是慢性阻塞性肺疾病(COPD)的重要病理特征。近年来,缺氧诱导因子 1-α(HIF-1α)作为缺氧诱导因子蛋白家族的一员受到关注。然而,HIF-1α与 COPD 气道重塑之间的潜在相关性尚不清楚。

目的

本研究探讨了 HIF-1α在 COPD 患者中的表达模式及其与气道重塑的关系。本研究旨在为临床识别改善 COPD 相关气道重塑的潜在治疗靶点提供新的见解。

患者和方法

共纳入 88 例患者,包括 28 例对照和 60 例 COPD 患者。采用多种染色方法观察气道组织的病理变化。免疫组织化学法检测气道组织中 HIF-1α和 MMP9(基质金属蛋白酶 9)的表达。酶联免疫吸附试验(ELISA)法检测血清中 HIF-1α和 MMP9 的浓度。对所有参与者进行计算机断层扫描(CT)气道参数测量,以评估气道重塑。分析血清 HIF-1α和 MMP9 浓度与气道参数的关系。

结果

COPD 患者气道结构染色显示与气道重塑相关的显著病理变化,包括混合纤毛和黏膜下纤维化。与对照组相比,人气道组织和血清中 HIF-1α和 MMP9 的表达均显著升高。胸部 CT 扫描显示出典型的气道重塑影像学特征和气道参数增加。

结论

研究结果提示 HIF-1α 表达增加与 COPD 气道重塑之间存在相关性。本研究提供了新的证据表明,HIF-1α 可能是 COPD 患者气道重塑的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/2734fd97fdfe/COPD-19-921-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/1d2ab71c717b/COPD-19-921-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/e1146c7d6c1d/COPD-19-921-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/6d59075c17ca/COPD-19-921-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/36957204064a/COPD-19-921-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/2734fd97fdfe/COPD-19-921-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/1d2ab71c717b/COPD-19-921-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/e1146c7d6c1d/COPD-19-921-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/6d59075c17ca/COPD-19-921-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/36957204064a/COPD-19-921-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72ab/11022883/2734fd97fdfe/COPD-19-921-g0005.jpg

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