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Tomas, L.* ; Edsfeldt, A.* ; Mollet, I.G.* ; Perisic Matic, L.* ; Prehn, C. ; Adamski, J. ; Paulsson-Berne, G.* ; Hedin, U.* ; Nilsson, J.* ; Bengtsson, E.* ; Gonçalves, I.* ; Björkbacka, H.*

Altered metabolism distinguishes high-risk from stable carotid atherosclerotic plaques.

Eur. Heart J. 39, 2301-2310 (2018)
Verlagsversion DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Aims Identification and treatment of the rupture prone atherosclerotic plaque remains a challenge for reducing the bur- den 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Atherosclerosis ; Carotid Plaque ; High-risk Plaque ; Metabolism ; Inflammation; Coronary-artery-disease; Atherogenesis; Vulnerability; Inflammation; Hif-1-alpha; Stroke
ISSN (print) / ISBN 0195-668X
e-ISSN 1522-9645
Quellenangaben Band: 39, Heft: 24, Seiten: 2301-2310 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Verlagsort Great Clarendon St, Oxford Ox2 6dp, England
Begutachtungsstatus Peer reviewed