The NF-kappa B signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation.

By L. Hajra, A. Evans, Mingyi Chen, S. Hyduk, T. Collins, M. Cybulsky. Proceedings of the National Academy of Sciences of the United States of America, 2000

637 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/125bb1db99c7e3dc062702c7d22d61df4ef9d01e

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In Cancer Research

1. Peter Libby
2. Ralph DeFronzo
3. A. Tedgui
4. Z. Mallat

In Immunology

1. Peter Libby
2. A. Tall
3. Karin E. Bornfeldt
4. A. Tedgui
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6. Z. Bloomgarden
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In Immunology and Allergy

1. Peter Libby

Citations in the corpus

• Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009 (2010, background): “The sensitising effect of VSMCs to angiotensin II is of particular importance, since hyperinsulinaemia doubles the ability of angiotensin II to transactivate NF-kB [120], a powerful nuclear transcription factor that activates multiple inflammatory pathways involved in atherogenesis [121, 122] and ca”
• Inflammation and insulin resistance. (2003, background): “ox-LDL also increases levels of the nuclear transcriptional activator, NF- B (46).”
• Research Progress on the Relationship between Atherosclerosis and Inflammation (2018, background): “After low density lipoprotein receptor (LDLR)−/− mice were fed a high-fat diet over an extended duration, the endothelium showed enhanced NF-κB activity, and the chance of local proximal aortic atherosclerosis increased [57].”
• KLF2 Is a Novel Transcriptional Regulator of Endothelial Proinflammatory Activation (2004, background): “These regions are known to be particularly susceptible to atherosclerotic lesion formation and exhibit increased levels of NF- B and VCAM-1 expression in animal models of atherosclerosis (16, 17).”
• Cytokines in atherosclerosis: pathogenic and regulatory pathways. (2006, background): “Enhanced endothelial activation of NF- B has been shown to occur in LDLr-deficient mice very early on following a high-fat diet, in regions of the proximal aorta with high probability for atherosclerotic lesion development (262).”
• Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, neutral): “20), E-selectin (168), PDGFs and their receptors (309, 566, 616), Cx43 (195, 314), Egr-1 (369), Ang-2 (574), cathepsin K (461), NF- B (48, 100, 234, 620), MMPs (29, 218), p70S6K (228), TLR-2 (399), PAK (437, 440), Shc (350), JNK (229), XBP-1 (647), HuR (487), GTPCH-1 (335), and HDAC3 (643), and decr”
• Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis (2016, positive): “Interestingly, in atherosclerosis-prone arterial geometries, endothelial NFκB seems to be primed for enhanced activation in response to systemic stimuli (Figure 2), such as bacterial endotoxin or hypercholesterolemia.(117) Recent studies suggest that NF-κB activation may also result in fundamental c”
• NF-κB: pivotal mediator or innocent bystander in atherogenesis? (2001, methodology): “Recently we demonstrated dramatic regional differences in NF-κB signal transduction in mouse aortic endothelial cells using specific antibody staining and en face confocal microscopy (43).”