Nf-kappab and AP-1 activation is associated with late lumen loss after porcine coronary angioplasty and antiproliferative beta-irradiation.
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Summary
Brachytherapy initially inhibits cell proliferation; however, cellular and molecular inflammatory processes (e.g. activation of NF-kappaB) are enhanced within the arterial wall and this proinflammatory side effect may be responsible for the observed delayed proliferation and the resulting lumen loss.
- Type
- dissertation
- Published
- 2007-07-01
- Cited by
- 7
- References
- 50
- Access
- Open access
- OpenAlex
- https://openalex.org/W17434466
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21260955
Keywords
Science education, Nature of Science, Mathematics education, Pedagogy, Learning sciences
References
- Transient Platelet Interaction Induces MCP-1 Production by Endothelial Cells via IκB Kinase Complex Activation
- Adventitial response to intravascular brachytherapy in a rabbit model of restenosis
- Late clinical events after clopidogrel discontinuation may limit the benefit of drug-eluting stents: an observational study of drug-eluting versus bare-metal stents.
- Macrophages contain 92-kd gelatinase (MMP-9) at the site of degenerated internal elastic lamina in temporal arteritis.
- Drug-eluting stent thrombosis: it's never too late
- Adenovirus-Mediated Gene Transfer of a Secreted Transforming Growth Factor-&bgr; Type II Receptor Inhibits Luminal Loss and Constrictive Remodeling After Coronary Angioplasty and Enhances Adventitial Collagen Deposition
- Inhibition of intimal hyperplasia after balloon injury in rat carotid artery model using cis-element ‘decoy’ of nuclear factor-kB binding site as a novel molecular strategy
- Interleukin-18-induced Human Coronary Artery Smooth Muscle Cell Migration Is Dependent on NF-κB- and AP-1-mediated Matrix Metalloproteinase-9 Expression and Is Inhibited by Atorvastatin*
- Intracoronary &bgr;-Radiation Exacerbates Long-Term Neointima Formation in Balloon-Injured Pig Coronary Arteries
- Vascular radiation in a drug-eluting stent world: it's not over till it's over.
- AP-1 as a regulator of cell life and death
- The effect of endovascular irradiation on platelet recruitment at sites of balloon angioplasty in pig coronary arteries.
- Pravastatin Limits Endothelial Activation after Irradiation and Decreases the Resulting Inflammatory and Thrombotic Responses
- Eplerenone Suppresses Constrictive Remodeling and Collagen Accumulation After Angioplasty in Porcine Coronary Arteries
- Remodeling rather than neointimal formation explains luminal narrowing after deep vessel wall injury: insights from a porcine coronary (re)stenosis model.
- Drug-eluting stents: are they really safe?
- Coronary in-stent restenosis following beta brachytherapy: a histopathological examination.
- Forkhead Transcription Factors Inhibit Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia*[boxs]
- Clinical demonstration that catheter-delivered ultrasound energy reverses arterial vasoconstriction.
- The Pro-atherogenic Cytokine Interleukin-18 Induces CXCL16 Expression in Rat Aortic Smooth Muscle Cells via MyD88, Interleukin-1 Receptor-associated Kinase, Tumor Necrosis Factor Receptor-associated Factor 6, c-Src, Phosphatidylinositol 3-Kinase, Akt, c-Jun N-terminal Kinase, and Activator Protein-1
Cited by
- Cardiovascular disease associated with radiotherapy: activation of nuclear factor kappa‐B
- Sustained inflammation due to nuclear factor-kappa B activation in irradiated human arteries.
- Vascular inflammation : Implications for microvascular reconstructive surgery after irradiation
- Long‐term clopidogrel administration following severe coronary injury reduces proliferation and inflammation via inhibition of nuclear factor‐kappaB and activator protein 1 activation in pigs
- Breast Cancer Survivors Undergoing Endocrine Therapy Have a Worrying Risk Factor Profile for Cardiovascular Diseases
- Nitric Oxide Synthase Uncoupling in Tumor Progression and Cancer Therapy
- Breast Cancer Survivors Undergoing Endocrine Therapy Have a Worrying Risk Factor Profile for Cardiovascular Diseases
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