Assessment of Risk Factors and Biomarkers of Cardiovascular Injury Induced by Environmental Exposure

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Integrative Metabolomics".

Deadline for manuscript submissions: closed (15 April 2022) | Viewed by 5224

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Guest Editor
Department of Medicine, Christina Lee Brown Envirome Institute, University of Louisville, Louisville, KY 40202, USA
Interests: particulate matter air pollution; volatile organic compounds; cardiovascular disease; endothelial progenitor cells; microplastics
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Special Issue Information

Abundant epidemiological, clinical, and laboratory studies have identified associations between environmental exposures and cardiovascular morbidity and mortality. However, there remains an incomplete mechanistic understanding of the basis of these associations. This Special Issue of Metabolites, titled “Assessment of Risk Factors and Biomarkers of Cardiovascular Injury Induced by Environmental Exposure”, will be dedicated to addressing these gaps in mechanistic understanding and to the identification of markers of preclinical cardiovascular disease in humans or animal models. Both original research and review papers will be considered for publication in this Special Issue. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the Special Issue website. Environmental exposures of any type (particles, gases, volatiles, metals) will be considered appropriate. Appropriate topics may include, but are not limited to: the identification of novel biomarkers, how such biomarkers contribute to cardiovascular disease, and methodological advances to assess exposure-induced biomarker changes.

Prof. Dr. Timothy E. O’Toole
Guest Editor

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Keywords

  • risk factors
  • biomarkers
  • mechanisms
  • cardiovascular disease
  • environmental exposures
  • interventional approaches

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Published Papers (1 paper)

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Research

15 pages, 2492 KiB  
Article
Dysregulated Metabolites Serve as Novel Biomarkers for Metabolic Diseases Caused by E-Cigarette Vaping and Cigarette Smoking
by Qixin Wang, Xiangming Ji and Irfan Rahman
Metabolites 2021, 11(6), 345; https://doi.org/10.3390/metabo11060345 - 29 May 2021
Cited by 11 | Viewed by 4671
Abstract
Metabolites are essential intermediate products in metabolism, and metabolism dysregulation indicates different types of diseases. Previous studies have shown that cigarette smoke dysregulated metabolites; however, limited information is available with electronic cigarette (e-cig) vaping. We hypothesized that e-cig vaping and cigarette smoking alters [...] Read more.
Metabolites are essential intermediate products in metabolism, and metabolism dysregulation indicates different types of diseases. Previous studies have shown that cigarette smoke dysregulated metabolites; however, limited information is available with electronic cigarette (e-cig) vaping. We hypothesized that e-cig vaping and cigarette smoking alters systemic metabolites, and we propose to understand the specific metabolic signature between e-cig users and cigarette smokers. Plasma from non-smoker controls, cigarette smokers, and e-cig users was collected, and metabolites were identified by UPLC-MS (ultra-performance liquid chromatography mass spectrometer). Nicotine degradation was activated by e-cig vaping and cigarette smoking with increased concentrations of cotinine, cotinine N-oxide, (S)-nicotine, and (R)-6-hydroxynicotine. Additionally, we found significantly decreased concentrations in metabolites associated with tricarboxylic acid (TCA) cycle pathways in e-cig users versus cigarette smokers, such as d-glucose, (2R,3S)-2,3-dimethylmalate, (R)-2-hydroxyglutarate, O-phosphoethanolamine, malathion, d-threo-isocitrate, malic acid, and 4-acetamidobutanoic acid. Cigarette smoking significant upregulated sphingolipid metabolites, such as d-sphingosine, ceramide, N-(octadecanoyl)-sphing-4-enine, N-(9Z-octadecenoyl)-sphing-4-enine, and N-[(13Z)-docosenoyl]-sphingosine, versus e-cig vaping. Overall, e-cig vaping dysregulated TCA cycle-related metabolites while cigarette smoking altered sphingolipid metabolites. Both e-cig and cigarette smoke increased nicotinic metabolites. Therefore, specific metabolic signatures altered by e-cig vaping and cigarette smoking could serve as potential systemic biomarkers for early pathogenesis of cardiopulmonary diseases. Full article
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