Discovery of potential biomarkers for human atherosclerotic abdominal aortic aneurysm through untargeted metabolomics and transcriptomics

• Published in: Journal of Zhejiang University. B. Science 2021-09, Vol.22 (9), p.733-745
• Main Authors: Ji, Lei, Chen, Siliang, Gu, Guangchao, Wang, Wei, Ren, Jinrui, Xu, Fang, Li, Fangda, Wu, Jianqiang, Yang, Dan, Zheng, Yuehong
• Format: Article
• Language: English
• Subjects: Aged; Aorta; Aortic Aneurysm, Abdominal - metabolism; Aortic aneurysms; Arteriosclerosis; Atherosclerosis; Atherosclerosis - metabolism; Biomarkers; Biomedical and Life Sciences; Biomedicine; D-Ribose; Female; Gene Expression Profiling - methods; Humans; Liquid chromatography; Male; Mass spectrometry; Mass spectroscopy; Metabolites; Metabolomics; Metabolomics - methods; Middle Aged; Pathogenesis; Patients; Research Article; Ribose; Risk analysis; Risk factors
• ISSN: 1673-1581; 1862-1783
• DOI: 10.1631/jzus.B2000713

Abdominal aortic aneurysm (AAA) and atherosclerosis (AS) have considerable similarities in clinical risk factors and molecular pathogenesis. The aim of our study was to investigate the differences between AAA and AS from the perspective of metabolomics, and to explore the potential mechanisms of differential metabolites via integration analysis with transcriptomics. Plasma samples from 32 AAA and 32 AS patients were applied to characterize the metabolite profiles using untargeted liquid chromatography-mass spectrometry (LC-MS). A total of 18 remarkably different metabolites were identified, and a combination of seven metabolites could potentially serve as a biomarker to distinguish AAA and AS, with an area under the curve (AUC) of 0.93. Subsequently, we analyzed both the metabolomics and transcriptomics data and found that seven metabolites, especially 2′-deoxy- d -ribose (2dDR), were significantly correlated with differentially expressed genes. In conclusion, our study presents a comprehensive landscape of plasma metabolites in AAA and AS patients, and provides a research direction for pathogenetic mechanisms in atherosclerotic AAA.