Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Jan Nilsson

Professor

Default user image.

Altered metabolism distinguishes high-risk from stable carotid atherosclerotic plaques

Author

  • Lukas Tomas
  • Andreas Edsfeldt
  • Inês G Mollet
  • Ljubica Perisic Matic
  • Cornelia Prehn
  • Jerzy Adamski
  • Gabrielle Paulsson-Berne
  • Ulf Hedin
  • Jan Nilsson
  • Eva Bengtsson
  • Isabel Gonçalves
  • Harry Björkbacka

Summary, in English

Aims: Identification and treatment of the rupture prone atherosclerotic plaque remains a challenge for reducing the burden of cardiovascular disease. The interconnection of metabolic and inflammatory processes in rupture prone plaques is poorly understood. Herein, we investigate associations between metabolite profiles, inflammatory mediators and vulnerability in carotid atherosclerotic plaques.

Methods and results: We collected 159 carotid plaques from patients undergoing endarterectomy and measured 165 different metabolites in a targeted metabolomics approach. We identified a metabolite profile in carotid plaques that associated with histologically evaluated vulnerability and inflammatory mediators, as well as presence of symptoms in patients. The distinct metabolite profiles identified in high-risk and stable plaques were in line with different transcription levels of metabolic enzymes in the two groups, suggesting an altered metabolism in high-risk plaques. The altered metabolic signature in high-risk plaques was consistent with a change to increased glycolysis, elevated amino acid utilization and decreased fatty acid oxidation, similar to what is found in activated leucocytes and cancer cells.

Conclusion: These results highlight a possible key role of cellular metabolism to support inflammation and a high-risk phenotype of atherosclerotic plaques. Targeting the metabolism of atherosclerotic plaques with novel metabolic radiotracers or inhibitors might therefore be valid future approaches to identify and treat the high-risk atherosclerotic plaque.

Department/s

  • Cardiovascular Research - Cellular Metabolism and Inflammation
  • EXODIAB: Excellence in Diabetes Research in Sweden
  • Cardiovascular Research - Immunity and Atherosclerosis
  • Cardiovascular Research - Translational Studies
  • Diabetes - Islet Cell Exocytosis
  • EpiHealth: Epidemiology for Health
  • Cardiovascular Research - Matrix and Inflammation in Atherosclerosis

Publishing year

2018-06-21

Language

English

Pages

2301-2310

Publication/Series

European Heart Journal

Volume

39

Issue

24

Document type

Journal article

Publisher

Oxford University Press

Topic

  • Cardiac and Cardiovascular Systems

Status

Published

Research group

  • Cardiovascular Research - Cellular Metabolism and Inflammation
  • Cardiovascular Research - Immunity and Atherosclerosis
  • Cardiovascular Research - Translational Studies
  • Diabetes - Islet Cell Exocytosis
  • Cardiovascular Research - Matrix and Inflammation in Atherosclerosis

ISBN/ISSN/Other

  • ISSN: 1522-9645