Macrophage ATP citrate lyase deficiency stabilizes atherosclerotic plaques
Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here,...
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| Published in: | Nature communications Vol. 11; no. 1; pp. 6296 - 15 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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London
Nature Publishing Group UK
08.12.2020
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
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| Abstract | Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques.
Inhibition of the metabolic enzyme ATP-citrate lyase can attenuate atherosclerosis by preventing dyslipidemia and potentially also by reducing macrophage-mediated inflammation. Here, the authors show that specific targeting of ACLY in macrophages results in more stable atherosclerotic plaques. |
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| AbstractList | Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques.Inhibition of the metabolic enzyme ATP-citrate lyase can attenuate atherosclerosis by preventing dyslipidemia and potentially also by reducing macrophage-mediated inflammation. Here, the authors show that specific targeting of ACLY in macrophages results in more stable atherosclerotic plaques. Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques. Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques.Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques. Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques. Inhibition of the metabolic enzyme ATP-citrate lyase can attenuate atherosclerosis by preventing dyslipidemia and potentially also by reducing macrophage-mediated inflammation. Here, the authors show that specific targeting of ACLY in macrophages results in more stable atherosclerotic plaques. Inhibition of the metabolic enzyme ATP-citrate lyase can attenuate atherosclerosis by preventing dyslipidemia and potentially also by reducing macrophage-mediated inflammation. Here, the authors show that specific targeting of ACLY in macrophages results in more stable atherosclerotic plaques. |
| ArticleNumber | 6296 |
| Author | van Weeghel, Michel Neele, Annette E. Kooij, Gijs Verberk, Sanne G. S. Broos, Jelle Y. Gijbels, Marion J. J. Sluimer, Judith C. de Vries, Helga E. Griffith, Guillermo R. Wellen, Kathryn E. Van den Bossche, Jan van Roomen, Cindy P. P. A. Lutgens, Esther van der Velden, Saskia Meinster, Elisa Molenaar, Douwe de Winther, Menno P. J. Prange, Koen H. M. Baardman, Jeroen Lakbir, Soufyan |
| Author_xml | – sequence: 1 givenname: Jeroen orcidid: 0000-0003-2822-8050 surname: Baardman fullname: Baardman, Jeroen organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 2 givenname: Sanne G. S. orcidid: 0000-0003-4509-4824 surname: Verberk fullname: Verberk, Sanne G. S. organization: Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Cancer Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam – sequence: 3 givenname: Saskia surname: van der Velden fullname: van der Velden, Saskia organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 4 givenname: Marion J. J. surname: Gijbels fullname: Gijbels, Marion J. J. organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Department of Pathology and Molecular Genetics, CARIM, Maastricht University – sequence: 5 givenname: Cindy P. P. A. surname: van Roomen fullname: van Roomen, Cindy P. P. A. organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 6 givenname: Judith C. orcidid: 0000-0002-0269-4582 surname: Sluimer fullname: Sluimer, Judith C. organization: Department of Pathology and Molecular Genetics, CARIM, Maastricht University, BHF Centre for Cardiovascular Sciences (CVS), University of Edinburgh – sequence: 7 givenname: Jelle Y. surname: Broos fullname: Broos, Jelle Y. organization: Department of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam, Leiden University Medical Center, Center for Proteomics & Metabolomics – sequence: 8 givenname: Guillermo R. orcidid: 0000-0002-3983-1499 surname: Griffith fullname: Griffith, Guillermo R. organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 9 givenname: Koen H. M. surname: Prange fullname: Prange, Koen H. M. organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 10 givenname: Michel orcidid: 0000-0002-4916-2866 surname: van Weeghel fullname: van Weeghel, Michel organization: Laboratory Genetic Metabolic Diseases, Amsterdam Cardiovascular sciences, Amsterdam UMC, University of Amsterdam, Core Facility Metabolomics, Amsterdam UMC, University of Amsterdam – sequence: 11 givenname: Soufyan surname: Lakbir fullname: Lakbir, Soufyan organization: Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Cancer Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam, Systems Bioinformatics, Vrije Universiteit Amsterdam – sequence: 12 givenname: Douwe surname: Molenaar fullname: Molenaar, Douwe organization: Systems Bioinformatics, Vrije Universiteit Amsterdam – sequence: 13 givenname: Elisa surname: Meinster fullname: Meinster, Elisa organization: Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Cancer Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam – sequence: 14 givenname: Annette E. surname: Neele fullname: Neele, Annette E. organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam – sequence: 15 givenname: Gijs surname: Kooij fullname: Kooij, Gijs organization: Department of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam – sequence: 16 givenname: Helga E. surname: de Vries fullname: de Vries, Helga E. organization: Department of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, MS Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam – sequence: 17 givenname: Esther orcidid: 0000-0002-2609-5744 surname: Lutgens fullname: Lutgens, Esther organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilians University – sequence: 18 givenname: Kathryn E. orcidid: 0000-0002-2281-0042 surname: Wellen fullname: Wellen, Kathryn E. organization: Department of Cancer Biology, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania – sequence: 19 givenname: Menno P. J. orcidid: 0000-0002-4038-6636 surname: de Winther fullname: de Winther, Menno P. J. email: m.dewinther@amsterdamumc.nl organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilians University – sequence: 20 givenname: Jan orcidid: 0000-0002-7852-2891 surname: Van den Bossche fullname: Van den Bossche, Jan email: j.vandenbossche@amsterdamumc.nl organization: Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Infection and Immunity, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Department of Molecular Cell Biology and Immunology, Amsterdam Cardiovascular Sciences, Cancer Center Amsterdam, Amsterdam UMC, Vrije Universiteit Amsterdam |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33293558$$D View this record in MEDLINE/PubMed |
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| Snippet | Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic... Inhibition of the metabolic enzyme ATP-citrate lyase can attenuate atherosclerosis by preventing dyslipidemia and potentially also by reducing... |
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| SubjectTerms | 101/58 13/2 13/21 13/31 13/51 14 14/1 38 38/88 38/91 45 631/250/2504/342 64/60 692/699/75 Aged Animals Apoptosis Apoptosis - immunology Arteriosclerosis Atherosclerosis ATP Citrate (pro-S)-Lyase - antagonists & inhibitors ATP Citrate (pro-S)-Lyase - deficiency ATP Citrate (pro-S)-Lyase - genetics ATP citrate lyase Biosynthesis Cell activation Cholesterol Cholesterol - biosynthesis Collagen Collagen - metabolism Deregulation Diet, High-Fat - adverse effects Disease Models, Animal Dyslipidemia Fatty acids Fatty Acids - biosynthesis Female Fibrosis Gene Expression Profiling Humanities and Social Sciences Humans Immune system Inflammatory diseases Lipidomics Lipids Lipogenesis - immunology Liver X receptors Liver X Receptors - metabolism Macrophage Activation Macrophages Macrophages - immunology Macrophages - metabolism Male Mice, Knockout multidisciplinary Necrosis - immunology Necrosis - pathology Phagocytosis Phenotypes Plaque, Atherosclerotic - drug therapy Plaque, Atherosclerotic - immunology Plaque, Atherosclerotic - pathology Plaques Receptor mechanisms Science Science (multidisciplinary) Transcription |
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| Title | Macrophage ATP citrate lyase deficiency stabilizes atherosclerotic plaques |
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