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REVIEW article

Front. Cell Dev. Biol.
Sec. Molecular and Cellular Pathology
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1446964
This article is part of the Research Topic Vascular- and Immuno-Metabolism as Drivers of Cardiovascular Disease: Insights Obtained from Omics Approaches View all 4 articles

Cellular metabolism changes in atherosclerosis and the impact of comorbidities

Provisionally accepted
Heidi Noels Heidi Noels 1*Yusang Dai Yusang Dai 2Carolina Junho Carolina Junho 2Luisa Schieren Luisa Schieren 2Julia Wollenhaupt Julia Wollenhaupt 2Judith Sluimer Judith Sluimer 3Emiel P. Van Der Vorst Emiel P. Van Der Vorst 2
  • 1 RWTH Aachen University, Institute for Molecular Cardiovascular Research, University Hospital RWTH Aachen, Aachen, Germany
  • 2 Institute for Molecular Cardiovascular Research, University Hospital RWTH Aachen, Aachen, Germany
  • 3 Maastricht University, Maastricht, Netherlands

The final, formatted version of the article will be published soon.

    Cell activation and nutrient dysregulation are common consequences of atherosclerosis and its preceding risk factors, such as hypertension, dyslipidemia, and diabetes. These diseases may also impact cellular metabolism and consequently cell function, and the other way around, altered cellular metabolism can impact disease development and progression through altered cell function. Understanding the contribution of altered cellular metabolism to atherosclerosis and how cellular metabolism may be altered by co-morbidities and atherosclerosis risk factors could support the development of novel strategies to lower the risk of CVD. Therefore, we briefly review disease pathogenesis and the principles of cell metabolic pathways, before detailing changes in cellular metabolism in the context of atherosclerosis and comorbidities.In the hypoxic, inflammatory and hyperlipidemic milieu of the atherosclerotic plaque riddled with oxidative stress, metabolism shifts to increase anaerobic glycolysis, the pentose-phosphate pathway and amino acid use. We elaborate on metabolic changes for macrophages, neutrophils, vascular endothelial cells, vascular smooth muscle cells and lymphocytes in the context of atherosclerosis and its co-morbidities hypertension, dyslipidemia, and diabetes. Since causal relationships of specific key genes in a metabolic pathway can be cell type-specific and comorbidity-dependent, the impact of cell-specific metabolic changes must be thoroughly explored in vivo, with a focus on also systemic effects. When cell-specific treatments become feasible, this information will be crucial for determining the best metabolic intervention to improve atherosclerosis and its interplay with co-morbidities.

    Keywords: Atherosclerosis, cell metabolism, Glycolysis, Fatty Acids, diabetes, Comorbidity

    Received: 10 Jun 2024; Accepted: 17 Jul 2024.

    Copyright: © 2024 Noels, Dai, Junho, Schieren, Wollenhaupt, Sluimer and Van Der Vorst. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Heidi Noels, RWTH Aachen University, Institute for Molecular Cardiovascular Research, University Hospital RWTH Aachen, Aachen, Germany

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.