ArticleFrontiers in cardiovascular medicine2018
Insights From Pre-Clinical and Clinical Studies on the Role of Innate Inflammation in Atherosclerosis Regression.
Article in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Interleukin-receptor antagonist and tumour necrosis factor inhibitors for the primary and secondary prevention of atherosclerotic cardiovascular diseases.The Cochrane database of systematic reviews · 2024Pooled it
- Inflammation and Immune Mechanisms in Atherosclerosis.Reviews in cardiovascular medicine · 2026Review
- Inflammation in atherosclerosis: a Big Idea that has underperformed so far.Current opinion in lipidology · 2025Review
- Research Advances and Application Progress on miRNAs in Exosomes Derived From M2 Macrophage for Tissue Injury Repairing.International journal of nanomedicine · 2025Review
- Changes in serum cholesterol loading capacity are linked to coronary atherosclerosis progression in rheumatoid arthritis.RMD open · 2024Observational
- Revisiting the role of IL-27 in obesity-related metabolic diseases: safeguard or perturbation?Frontiers in immunology · 2024Review
- Trehalose promotes atherosclerosis regression in female mice.Frontiers in cardiovascular medicine · 2024Article
- A Lipid-Structured Model of Atherosclerotic Plaque Macrophages with Lipid-Dependent Kinetics.Bulletin of mathematical biology · 2023Article
- PACAP regulates VPAC1 expression, inflammatory processes and lipid homeostasis in M1- and M2-macrophages.Frontiers in cardiovascular medicine · 2023Article
- Haematological Parameters in People with Atherosclerotic Cardiovascular Disease versus Those Who are Only at Risk for Cardiovascular Disease: A Comparative Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Macrophage polarization as a potential therapeutic target for atherosclerosis: a dynamic stochastic modelling study.Royal Society open science · 2022Article
- Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice.Scientific reports · 2022Article
- IL-4 polarized human macrophage exosomes control cardiometabolic inflammation and diabetes in obesity.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Survey of Approaches for Investigation of Atherosclerosis In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mitogen and Stress-Activated Kinases 1 and 2 Mediate Endothelial Dysfunction.International journal of molecular sciences · 2021Article
- Reshaping of the gastrointestinal microbiome alters atherosclerotic plaque inflammation resolution in mice.Scientific reports · 2021Article
- Wnt signaling enhances macrophage responses to IL-4 and promotes resolution of atherosclerosis.eLife · 2021Article
- Short-Term Acyl-CoA:Cholesterol Acyltransferase Inhibition, Combined with Apoprotein A1 Overexpression, Promotes Atherosclerosis Inflammation Resolution in Mice.Molecular pharmacology · 2021Article
- Huang-Lian-Jie-Du Decoction Attenuates Atherosclerosis and Increases Plaque Stability in High-Fat Diet-Induced ApoEFrontiers in physiology · 2021Article
- Acarbose attenuates migration/proliferation via targeting microRNA-143 in vascular smooth muscle cells under diabetic conditions.Journal of food and drug analysis · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis, the underlying cause of coronary artery (CAD) and other cardiovascular diseases, is initiated by macrophage-mediated immune responses to lipoprotein and cholesterol accumulation in artery walls, which result in the formation of plaques. Unlike at other sites of inflammation, the immune response becomes maladaptive and inflammation fails to resolve. The most common treatment for reducing the risk from atherosclerosis is low density lipoprotein cholesterol (LDL-C) lowering. Studies have shown, however, that while significant lowering of LDL-C reduces the risk of heart attacks to some degree, there is still residual risk for the majority of the population. We and others have observed "residual inflammatory risk" of atherosclerosis after plasma cholesterol lowering in pre-clinical studies, and that this phenomenon is clinically relevant has been dramatically reinforced by the recent Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) trial. This review will summarize the role of the innate immune system, specifically macrophages, in atherosclerosis progression and regression, as well as the pre-clinical and clinical models that have provided significant insights into molecular pathways involved in the resolution of plaque inflammation and plaque regression. Partnered with clinical studies that can be envisioned in the post-CANTOS period, including progress in developing targeted plaque therapies, we expect that pre-clinical studies advancing on the path summarized in this review, already revealing key mechanisms, will continue to be essential contributors to achieve the goals of dampening plaque inflammation and inducing its resolution in order to maximize the therapeutic benefits of conventional risk factor modifications, such as LDL-C lowering.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.