ArticleMediators of inflammation2014
Silence of NLRP3 suppresses atherosclerosis and stabilizes plaques in apolipoprotein E-deficient mice.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 146 citations in OpenAlex.
- Unravelling the Therapeutic Potential of Cysteine for Cardiovascular Health.International journal of molecular sciences · 2026Review
- Macrophage-derived galectin-3 contributes to pyroptosis, apoptosis and necroptosis through TLR4/MyD88/NF-κB/NLRP3 during atherosclerosis.Clinical and translational medicine · 2026Article
- Enhancing Mitophagy with PEP-1-CAT Attenuates Vascular Inflammation and Atherogenesis in Mice.Inflammation · 2026Article
- Targeting pyroptosis in atherosclerosis: emerging pharmacologic strategies and natural compound-based therapeutics-a narrative review.International journal of clinical pharmacy · 2026Review
- Exercise Alleviates Atherosclerosis Through the Modulation of the NLRP3 Inflammasome.Current molecular medicine · 2026Review
- Analysis of the Correlation Between Cuproptosis and Instability of Atherosclerotic Plaques.Biomedicines · 2025Article
- Caspase-1 inhibition mitigates neonatal hyperoxia-induced vascular and cardiopulmonary inflammation in neonatal rats.Clinical science (London, England : 1979) · 2025Article
- Emodin Suppresses NLRP3/GSDMD-induced Inflammation via the TLR4/MyD88/NF-κB Signaling Pathway in Atherosclerosis.Cardiovascular drugs and therapy · 2025Article
- Gene Therapy Approaches for Atherosclerosis Focusing on Targeting Lipid Metabolism and Inflammation.International journal of molecular sciences · 2025Review
- NLRP3, conveyed via extracellular vesicles from metabolic syndrome patients, is involved in atherosclerosis development.Cell communication and signaling : CCS · 2025Article
- NLRP3 Inflammasome Inhibition by the Novel Bispecific Antibody InflamAb Attenuates Atherosclerosis in Apolipoprotein E-Deficient Mice.JACC. Basic to translational science · 2025Article
- USP22 enhances atherosclerotic plaque stability and macrophage efferocytosis by stabilizing PPARγ.Communications biology · 2025Article
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Inflammatory Pathways in Coronary Artery Disease: Which Ones to Target for Secondary Prevention?Cells · 2025Review
- The Potential Impact of SGLT2-I in Diabetic Foot Prevention: Promising Pathophysiologic Implications, State of the Art, and Future Perspectives-A Narrative Review.Medicina (Kaunas, Lithuania) · 2024Review
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets.Nature reviews. Cardiology · 2024Review
- Moving from lipids to leukocytes: inflammation and immune cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Recent progress of endoplasmic reticulum stress in the mechanism of atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- HFD-exacerbated Metabolic Side Effects of Olanzapine Are Suppressed by ER Stress Inhibitor.Current medical science · 2023Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe role of the NLRP3 inflammasome in atherosclerosis remains controversial. The aim of this study was to determine whether inhibition of NLRP3 signaling by lentivirus-mediated RNA interference could reduce atherosclerosis and stabilizes plaques. We also tried to explore the mechanisms of the impact of NLRP3 inflammasome on atherosclerosis.
methodsApolipoprotein E-deficient mice aged 8 weeks were fed a high-fat diet and were injected with NLRP3 interfering or mock viral suspension after 4 weeks. Lentivirus transfer was repeated in 2 weeks. Four weeks after the first lentivirus injection, we evaluated the effects of NLRP3 gene silencing on plaque composition and stability and on cholesterol efflux and collagen metabolism, by histopathologic analyses and real-time PCR.
resultsGene silence of NLRP3 prevented plaques progression and inhibited inductions of proinflammatory cytokines. Moreover, this RNA interference reduced plaque content of macrophages and lipid, and increased plaque content of smooth muscle cells and collagen, leading to the stabilizing of atherosclerotic plaques.
conclusionsNLRP3 inflammasomes may play a vital role in atherosclerosis, and lentivirus-mediated NLRP3 silencing would be a new strategy to inhibit plaques progression and to reduce local inflammation.
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