Atherosclerosis: current pathogenesis and therapeutic options
Abstract
Coronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.
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Modified lipids activate intimal inflammatory cells to secrete pro-inflammatory chemokines and cytokines, promoting further recruitment of myeloid inflammatory cells, particularly inflammatory monocytes, in mice and humans.
“The modified lipids then activate the inflammatory cells present in the intima, which respond by secreting pro-inflammatory chemokines and cytokines that in turn activate circulating leukocytes and the local endothelial cells, thereby promoting further recruitment of inflammatory cells of myeloid origin, particularly a specific subset of circulating monocytes with inflammatory potential, as shown”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [18]
Inflammation and hypercholesterolemia are the 2 key etiological factors for atherosclerosis.
“Inflammation and hypercholesterolemia are the 2 key etiological factors for atherosclerosis.”
From <i>Akkermansia Muciniphila</i> Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in <i>Apoe</i> <sup>−/−</sup> Mice (2016) · cites this paper as [39]
Animal-based studies have reported effectiveness of several anti-inflammatory interventions in alleviating atherosclerosis, but clinical implications remain to be confirmed.
“Animal-based studies have reported the effectiveness of several anti-inflammatory interventions in alleviating atherosclerosis, including the CD40-TNF receptor-associated factor 6-specific blockade and IL-1 neutralization, but clinical implications of these findings remain to be confirmed.”
From <i>Akkermansia Muciniphila</i> Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in <i>Apoe</i> <sup>−/−</sup> Mice (2016) · cites this paper as [39]
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Vessel Wall–Embedded Dendritic Cells Induce T-Cell Autoreactivity and Initiate Vascular Inflammation
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Chemokine Receptor 7 Knockout Attenuates Atherosclerotic Plaque Development
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Macrophage Migration Inhibitory Factor: A Noncanonical Chemokine Important in Atherosclerosis
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Measles Virus Nucleoprotein Induces a Regulatory Immune Response and Reduces Atherosclerosis in Mice
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Inflammasomes: mechanism of action, role in disease, and therapeutics
Guo, H., Callaway, J. B., & Ting, J. P.-Y. (2015) · Nature Medicine · doi:10.1038/nm.3893 · Cited by 3,340 · see citing works
Macrophages in atherosclerosis: a dynamic balance
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Borén, J., Chapman, M. J., Krauss, R. M., Packard, C. J., Bentzon, J. F., Binder, C. J., Daemen, M. J., Demer, L. L., Hegele, R. A., Nicholls, S. J., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz962 · Cited by 1,601 · see citing works
Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
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Senescent cells: an emerging target for diseases of ageing
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Senescent intimal foam cells are deleterious at all stages of atherosclerosis
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Chronic variable stress activates hematopoietic stem cells
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Regulation of lipid stores and metabolism by lipophagy
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Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?
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Partners in crime: neutrophils and monocytes/macrophages in inflammation and disease
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Immunotherapy for cardiovascular disease
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Self-citationSenescent cells: a therapeutic target for cardiovascular disease
Childs, B. G., Li, H., & van Deursen, J. M. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95146 · Cited by 192 · see citing works
Neurovascular Dysfunction in Vascular Dementia, Alzheimer's and Atherosclerosis
Shabir, O., Berwick, J., & Francis, S. E. (2018) · BMC Neuroscience · doi:10.1186/s12868-018-0465-5 · Cited by 191 · see citing works
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The Biological Role of Inflammation in Atherosclerosis
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Annexin A1 Counteracts Chemokine-Induced Arterial Myeloid Cell Recruitment
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Mitochondrial DNA damage and atherosclerosis
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“These plaques can rupture, potentially leading to vessel occlusion and clinical sequelae such as heart attacks and strokes [1].”
BackgroundAn early-stage atherosclerosis research model based on microfluidics
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Noncoding RNAs regulate NF-κB signaling to modulate blood vessel inflammation
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Eating the dead to keep atherosclerosis at bay
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“Even as new proinflammatory and anti-inflammatory pathways are being discovered, the foundational role of LDL in atherogenesis remains axiomatic.(12)”
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Bai, Z., Yang, P., Yu, F., Li, Z., Yao, Z., Martinez, J., Li, M., & Xu, H. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-04562-w · Cited by 43 · see citing works
“INTRODUCTION Aging is one of the major risk factors for many diseases [1], and the development of methods to intervene in aging will significantly reduce the risk of a series of age-related diseases such as cardiovascular and cerebrovascular diseases [2, 3], cancer [4], and Alzheimer’s disease [5].”
BackgroundThe macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis
Sallam, T., Ito, A., Rong, X., Kim, J., van Stijn, C., Chamberlain, B. T., Jung, M. E., Chao, L. C., Jones, M., Gilliland, T., et al. (2014) · Journal of Lipid Research · doi:10.1194/jlr.m047548 · Cited by 30 · see citing works
An overview on nanoplatforms for statins delivery: Perspectives for safe and effective therapy
Etemad, L., Salmasi, Z., Moosavian Kalat, S. A., Moshiri, M., Zamanian, J., Kesharwani, P., & Sahebkar, A. (2023) · Environmental Research · doi:10.1016/j.envres.2023.116572 · Cited by 18 · see citing works
- Authors
- Weber, C., & Noels, H.
- Affiliations
- Ludwig-Maximilians-Universität München (DE)
- RWTH Aachen University (DE)
- Corresponding author
- Weber, Christian
- Venue
- Nature Medicine
- Published
- 2011-11
- Volume
- 17
- Issue
- 11
- Pages
- 1410-1422
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2094629035
- Cited by
- 2,203
- References
- 135
- Citations by year
- 2026: 66 · 2025: 119 · 2024: 133 · 2023: 137 · 2022: 190 · 2021: 189 · 2020: 177 · 2019: 181 · 2018: 154 · 2017: 126 · 2016: 158 · 2015: 162 · 2014: 171 · 2013: 141 · 2012: 94
- FWCI
- 11.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Fondation Leducq
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- atherosclerosis, coronary artery disease, lipid metabolism, chronic inflammation, immune response, leukocyte migration, chemokines, chemokine receptors, genetic profiling, lipid-lowering therapy, anti-inflammatory therapy, atherogenesis
- MeSH terms
- B-Lymphocytes, Coronary Artery Disease, Dendritic Cells, Homeostasis, Humans, Immunity, Innate, Inflammation, Neutrophils, T-Lymphocytes, Chemokines, Receptors, Chemokine, Atherosclerosis, Lipid Metabolism, Adaptive Immunity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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