ArticleThe Journal of clinical investigation2003
Inhibition of NF-kappaB activation in macrophages increases atherosclerosis in LDL receptor-deficient mice.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.
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Who cites it
147 citing papers in PubMed, 312 citations in OpenAlex.
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- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Oxalate as an Emerging Contributor to Cardiovascular Disease: Links to Inflammation, Immunity, and Oxidative Stress.Nutrients · 2026Review
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.bioRxiv : the preprint server for biology · 2025Article
- Identification of a PRDM1-regulated T cell network to regulate atherosclerotic plaque inflammation.Genome medicine · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- The new perspective on understanding the mechanisms of cardiovascular diseases development.Scientific reports · 2025Article
- Cardiovascular protein profiling in patients with first-episode psychosis.Schizophrenia (Heidelberg, Germany) · 2025Article
- TFEB-mediated proinflammatory response in murine macrophages induced by acute Alpha7 nicotinic receptor activation.Journal of leukocyte biology · 2025Article
- An NF-kB/TNF-alpha signalling feedback loop acts to coordinate tissue regeneration and macrophage behaviour in zebrafish.NPJ Regenerative medicine · 2025Article
- IL-10-Directed Cancer Immunotherapy: Preclinical Advances, Clinical Insights, and Future Perspectives.Cancers · 2025Review
- Neutrophil Extracellular Traps in Atherosclerosis: Research Progress.International journal of molecular sciences · 2025Review
- Inflammation in atherosclerosis: pathophysiology and mechanisms.Cell death & disease · 2024Review
- IL-1β Inhibition Partially Negates the Beneficial Effects of Diet-Induced Atherosclerosis Regression in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Treatment of advanced atherosclerotic mice with ABT-263 reduced indices of plaque stability and increased mortality.JCI insight · 2024Article
- IL-1β inhibition partially negates the beneficial effects of diet-induced lipid lowering.bioRxiv : the preprint server for biology · 2023Article
- The role of autophagy in cardiovascular disease: Cross-interference of signaling pathways and underlying therapeutic targets.Frontiers in cardiovascular medicine · 2023Review
- Smooth muscle cell specific NEMO deficiency inhibits atherosclerosis in ApoEScientific reports · 2022Article
- Lipid metabolism in autoimmune rheumatic disease: implications for modern and conventional therapies.The Journal of clinical investigation · 2022Review
87 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is now generally accepted as a chronic inflammatory condition. The transcription factor NF-kappaB is a key regulator of inflammation, immune responses, cell survival, and cell proliferation. To investigate the role of NF-kappaB activation in macrophages during atherogenesis, we used LDL receptor-deficient mice with a macrophage-restricted deletion of IkappaB kinase 2 (IKK2), which is essential for NF-kappaB activation by proinflammatory signals. These mice showed increased atherosclerosis as quantified by lesion area measurements. In addition, the lesions were more advanced and showed more necrosis and increased cell number in early lesions. Southern blotting revealed that deletion of IKK2 was approximately 65% in macrophages, coinciding with a reduction of 50% in NF-kappaB activation, as compared with controls. In both groups, the expression of differentiation markers, uptake of bacteria, and endocytosis of modified LDL was similar. Upon stimulation with LPS, production of TNF was reduced by approximately 50% in IKK2-deleted macrophages. Interestingly, we also found a major reduction in the anti-inflammatory cytokine IL-10. Our data show that inhibition of the NF-kappaB pathway in macrophages leads to more severe atherosclerosis in mice, possibly by affecting the pro- and anti-inflammatory balance that controls the development of atherosclerosis.
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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.