ArticleCirculation research2015
Identification of a non-growth factor role for GM-CSF in advanced atherosclerosis: promotion of macrophage apoptosis and plaque necrosis through IL-23 signaling.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
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- Human Coronary Plaque T Cells Are Clonal and Cross-React to Virus and Self.Circulation research · 2022Article
- Intravesical immunotherapy with a GM-CSF armed oncolytic vesicular stomatitis virus improves outcome in bladder cancer.Molecular therapy oncolytics · 2022Article
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- Exploring the Diverse Immune and Genetic Landscape of Psoriatic Arthritis.Journal of clinical medicine · 2021Review
- Cardiovascular Safety of Biologics Targeting Interleukin (IL)-12 and/or IL-23: What Does the Evidence Say?American journal of clinical dermatology · 2021Review
- MiR-140-5p inhibits oxidized low-density lipoprotein-induced oxidative stress and cell apoptosis via targeting toll-like receptor 4.Gene therapy · 2021Article
- Myeloid-associated lipin-1 transcriptional co-regulatory activity is atheroprotective.Atherosclerosis · 2021Article
- Morphine enhances LPS-induced macrophage apoptosis through a PPARγ-dependent mechanism.Experimental and therapeutic medicine · 2021Article
- Limited proliferation capacity of aortic intima resident macrophages requires monocyte recruitment for atherosclerotic plaque progression.Nature immunology · 2020Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
rationaleGranulocyte macrophage colony-stimulating factor (GM-CSF, Csf2) is a growth factor for myeloid-lineage cells that has been implicated in the pathogenesis of atherosclerosis and other chronic inflammatory diseases. However, the role of GM-CSF in advanced atherosclerotic plaque progression, the process that gives rise to clinically dangerous plaques, is unknown.
objectiveTo understand the role of GM-CSF in advanced atherosclerotic plaque progression. METHODS AND
resultsLdlr(-/-) mice and Csf2(-/-)Ldlr(-/-) mice were fed a Western-type diet for 12 weeks, and then parameters of advanced plaque progression in the aortic root were quantified. Lesions from the GM-CSF-deficient mice showed a substantial decrease in 2 key hallmarks of advanced atherosclerosis, lesional macrophage apoptosis and plaque necrosis, which indicates that GM-CSF promotes plaque progression. Based on a combination of in vitro and in vivo studies, we show that the mechanism involves GM-CSF-mediated production of interleukin-23, which increases apoptosis susceptibility in macrophages by promoting proteasomal degradation of the cell survival protein Bcl-2 (B-cell lymphoma 2) and by increasing oxidative stress.
conclusionsIn low-density lipoprotein-driven atherosclerosis in mice, GM-CSF promotes advanced plaque progression by increasing macrophage apoptosis susceptibility. This action of GM-CSF is mediated by its interleukin-23-inducing activity rather than its role as a growth factor.
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