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Large Scale Non-targeted Metabolomic Profiling of Serum by Ultra Performance Liquid Chromatography-Mass Spectrometry UPLC-MS
Published on: March 14, 2013
Metabolomic analysis of serum from pure coronary artery ectasia patients based on UPLC-QE/MS technique
Zhe Cao1, Jinyu Wang1, Zuyi Weng2
1Department of Cardiology, Nanjing Medical University Second Affiliated Hospital, Nanjing Medical University, Nanjing 210011, China.
Insights
This study identified ten unique serum metabolites in coronary artery ectasia (CAE) patients, offering potential for early diagnosis. These findings shed light on the metabolic pathways involved in CAE, including amino acid and energy metabolism.
Area of Science:
- Cardiovascular Research
- Metabolomics
- Biomarker Discovery
Background:
- Coronary artery ectasia (CAE) is a condition of abnormal coronary artery dilation with unclear pathophysiology.
- Understanding the metabolic differences in CAE is crucial for diagnosis and treatment.
Purpose of the Study:
- To investigate distinct serum metabolomic profiles in pure CAE patients compared to mixed CAE and healthy controls.
- To identify potential biomarkers for early diagnosis of pure CAE.
Main Methods:
- Serum samples from 14 pure CAE, 12 mixed CAE, and 14 control patients were analyzed using untargeted ultra-high performance liquid chromatography-mass spectrometry.
- Key biomarkers including ICAM-1, VEGF, ROS, and glutathione were quantified.
Main Results:
- Ten serum metabolites, including 1-cyano-2-hydroxy-3-butene and D-alanine, differentiated pure CAE patients.
- Metabolic pathways implicated include amino acid metabolism, sphingolipid dysfunction, and oxidative stress.
- Elevated ICAM-1, VEGF, and ROS, with decreased glutathione, were observed in CAE patients, correlating with specific metabolites.
Conclusions:
- This study presents the first metabolomic profile differentiating pure CAE from mixed CAE and controls.
- Ten novel biomarkers were identified, potentially enabling early diagnosis of pure CAE.
- The findings enhance understanding of pure CAE pathogenesis, highlighting systemic inflammation and oxidative stress.
Background:
Coronary artery ectasia (CAE) is a cardiovascular disorder characterized by abnormal coronary artery dilation and disturbed coronary flow. The exact pathophysiology of CAE is still unclear. We aimed to investigate differences in metabolomic profiles between CAE patients and healthy controls.
Methods:
Radial artery blood samples were collected from 14 pure CAE patients, 12 mixed CAE patients with atherosclerosis, and 14 controls with normal angiography. Differential serum metabolites were analyzed by untargeted ultra-high performance liquid chromatography-mass spectrometry. Serum ICAM-1, VEGF, ROS, and glutathione levels were also measured.
Results:
Ten metabolites distinguished pure CAE patients from controls and mixed CAE, including 1-cyano-2-hydroxy-3-butene, 2,3-dihydro-6-methyl-5-(5-methyl-2-furanyl)-1H-pyrrolizine, 2-propionylpyrrole, 2-pyrrolidinone, 3-(2-furanylmethylene)pyrrolidine, D-alanine, furanofukinin, o-ethyltoluene, rotundine A, and SM(d18:1/18:1(9Z)). Related metabolic pathways include amino acid metabolism, sphingolipid dysfunction, energy metabolism, mitochondrial dysfunction, and oxidative stress. Serum concentrations of ICAM-1, VEGF and ROS were significantly elevated in CAE patients compared to controls, while glutathione decreased significantly in CAE patients. Moreover, ICAM-1 levels were negatively correlated with 2-propionylpyrrole, and VEGF levels were negatively correlated with SM(d18:1/18:1(9Z)), while GSH and ROS levels were correlated with the abundance of SM(d18:1/18:1(9Z)), further confirming systemic inflammation and oxidative stress in CAE.
Conclusions:
This is the first report describing differential serum metabolomic profiles of pure CAE patients compared to mixed CAE and healthy controls, which revealed 10 potential biomarkers that can provide an early diagnosis of pure CAE. These discriminatory metabolites and related metabolic pathways can help to better understand the pathogenesis of pure CAE.
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