Suppr超能文献

慢性阻塞性肺疾病肺组织中靶向代谢组学的变化

Changes in targeted metabolomics in lung tissue of chronic obstructive pulmonary disease.

作者信息

Feng Yi, Xie Meiqin, Liu Qi, Weng Jiali, Wei Liangyu, Chung Kian Fan, Adcock Ian M, Chang Qing, Li Mengnan, Huang Yan, Zhang Hai, Li Feng

机构信息

Department of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Experimental Studies, Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, UK.

出版信息

J Thorac Dis. 2023 May 30;15(5):2544-2558. doi: 10.21037/jtd-22-1731. Epub 2023 May 22.

Abstract

BACKGROUND

Chronic obstructive pulmonary disease (COPD) is a common chronic lung disease and its incidence is steadily increasing. COPD patients and mouse models of COPD share some similarities in lung pathology and physiology. We performed this study to explore the potential metabolic pathways involved in the pathogenesis of COPD and to discover the COPD-associated biomarkers. Furthermore, we aimed to examine how much the mouse model of COPD was similar and different to human COPD in terms of the altered metabolites and pathways.

METHODS

Twenty human lung tissue samples (ten COPD and ten controls) and twelve mice lung tissue samples (six COPD and six controls) were analyzed by targeted HM350 metabolomics, and multivariate and pathway analysis were performed by Kyoto Encyclopedia of Genes and Genomes (KEGG) database.

RESULTS

The counts of many metabolites such as amino acids, carbohydrates and carnitines were changed in both COPD patients and mice compared to controls, respectively. While lipid metabolism was changed only in COPD mice. After KEGG analysis, we found these altered metabolites involved in COPD through aging, apoptosis, oxidative stress and inflammation pathways.

CONCLUSIONS

The expressions of metabolites changed in both COPD patients and cigarette smoke exposed (CS-exposed) mice. And there were also some differences between COPD patients and mouse models due to the differences between species. Our study suggested the dysregulation in amino acid metabolism, energy production pathway and perhaps lipid metabolism may be significantly related to the pathogenesis of COPD.

摘要

背景

慢性阻塞性肺疾病(COPD)是一种常见的慢性肺部疾病,其发病率正在稳步上升。COPD患者与COPD小鼠模型在肺部病理和生理方面存在一些相似之处。我们开展这项研究,以探索参与COPD发病机制的潜在代谢途径,并发现与COPD相关的生物标志物。此外,我们旨在研究在代谢物和途径改变方面,COPD小鼠模型与人类COPD的异同程度。

方法

通过靶向HM350代谢组学分析20个人类肺组织样本(10例COPD患者和10例对照)和12只小鼠肺组织样本(6只COPD小鼠和6只对照),并通过京都基因与基因组百科全书(KEGG)数据库进行多变量和途径分析。

结果

与对照组相比,COPD患者和小鼠体内许多代谢物的数量均发生了变化,如氨基酸、碳水化合物和肉碱。而脂质代谢仅在COPD小鼠中发生改变。经KEGG分析,我们发现这些改变的代谢物通过衰老、细胞凋亡、氧化应激和炎症途径参与COPD的发病过程。

结论

COPD患者和暴露于香烟烟雾(CS暴露)的小鼠体内代谢物的表达均发生了变化。由于物种差异,COPD患者与小鼠模型之间也存在一些差异。我们的研究表明,氨基酸代谢、能量产生途径以及可能的脂质代谢失调可能与COPD的发病机制密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0507/10267913/0945a64877e9/jtd-15-05-2544-f1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验