Cited by 218NF-κB Signaling PathwaysAtherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin Effects

The nuclear factor-kappa B pathway in atherosclerosis: a potential therapeutic target for atherothrombotic vascular disease

Pamukcu, Burak, Lip, Gregory Y.H., Shantsila, Eduard·2011·Thrombosis Research

Abstract

Nuclear factor kappa B (NFκB) is a transcription factor belonging to 'Rel' family that represents a crucial intracellular signal transduction system involved in several inflammatory diseases including atherosclerosis. Activation of NFκB mediated signal transduction has been established at different stages of atherosclerosis, beginning from plaque formation to its destabilization and rupture. The NFκB pathway is also involved in angiogenic, apoptotic and neoplastic processes. Experimental studies indicate that inhibition of these pathway may reduce inflammatory burden. The development of natural or pharmaceutical, selective and specific inhibitors of NFκB pathway over IκB kinase α or β, may ultimately prove to be promising anti-atherosclerotic, anti-inflammatory, antiangiogenic and antiapoptotic therapeutic instruments that could potentially reduce inflammation, attenuate atherogenesis and prevent its complications.

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Registry

Crossref · 10.1016/j.thromres.2011.03.025

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110 of 110 references verified0 citation errors · 0 not checkable

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  • Inflammatory signals such as LPS, pro-inflammatory cytokines, reactive oxygen species, advanced glycation end products, and oxidized LDL cause IKKβ phosphorylation; this phosphorylates IκBα, leading to its ubiquitination and degradation, which releases NF-κB to enter the nucleus and induce pro-inflammatory genes.

    “Extracellular inflammatory signals including lipopolysaccharide (LPS), pro-inflammatory cytokines, reactive oxygen species, advanced glycation end products, and oxidized low-density lipoprotein trigger the phosphorylation of IKKβ, which in turn phosphorylates IκBα for ubiquitination and degradation by proteasome [13–18].”

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Authors
Pamukcu, B., Lip, G. Y. H., & Shantsila, E.
Affiliations
Birmingham City Hospital (GB)
Corresponding author
Shantsila, Eduard
Venue
Thrombosis Research
Publisher
Elsevier BV
Published
2011-08
Volume
128
Issue
2
Pages
117-123
ISSN
0049-3848 (ISSN-L)
OpenAlex
W2054805566
Cited by
218
References
110
Citations by year
2026: 3 · 2025: 18 · 2024: 14 · 2023: 15 · 2022: 14 · 2021: 18 · 2020: 16 · 2019: 22 · 2018: 22 · 2017: 11 · 2016: 16 · 2015: 20 · 2014: 12 · 2013: 10 · 2012: 7
FWCI
0.67
Type
journal article
Language
en
Open access
closed
Locations
  • Thrombosis Research (publishedVersion)
  • PubMed (publishedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
NF-κB signaling, atherosclerosis, IκB kinase inhibitors, inflammation, plaque rupture, atherogenesis, angiogenesis, apoptosis, anti-inflammatory therapy
MeSH terms
Animals, Humans, Signal Transduction, NF-kappa B, Inflammation Mediators, Atherosclerosis

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