ArticleJournal of the American Heart Association2013
Smooth muscle-selective inhibition of nuclear factor-κB attenuates smooth muscle phenotypic switching and neointima formation following vascular injury.
Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 80 citations in OpenAlex.
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- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
- SGLT2 inhibitor improves the prognosis of patients with coronary heart disease and prevents in-stent restenosis.Frontiers in cardiovascular medicine · 2023Review
- Modified Yuejuwan Inhibited Cholesterol Accumulation and Inflammation in THP-1 Macrophage-Derived Foam Cells by Inhibiting the Activity of the TRIM37/TRAF2/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Vascular smooth muscle cells in atherosclerosis: time for a re-assessment.Cardiovascular research · 2021Review
- Research advance of Nrf2 on atherosclerosis by regulating vascular smooth muscle cell.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- Targeting the phenotypic switch of vascular smooth muscle cells to tackle atherosclerosis.Atherosclerosis · 2021Article
- Eosinophils Protect Mice From Angiotensin-II Perfusion-Induced Abdominal Aortic Aneurysm.Circulation research · 2021Article
- Epigenetic Regulation of Vascular Smooth Muscle Cell Phenotype Switching in Atherosclerotic Artery Remodeling: A Mini-Review.Frontiers in genetics · 2021Review
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVascular proliferative diseases such as atherosclerosis are inflammatory disorders involving multiple cell types including macrophages, lymphocytes, endothelial cells, and smooth muscle cells (SMCs). Although activation of the nuclear factor-κB (NF-κB) pathway in vessels has been shown to be critical for the progression of vascular diseases, the cell-autonomous role of NF-κB within SMCs has not been fully understood. METHODS AND
resultsWe generated SMC-selective truncated IκB expressing (SM22α-Cre/IκBΔN) mice, in which NF-κB was inhibited selectively in SMCs, and analyzed their phenotype following carotid injury. Results showed that neointima formation was markedly reduced in SM22α-Cre/IκBΔN mice after injury. Although vascular injury induced downregulation of expression of SMC differentiation markers and myocardin, a potent activator of SMC differentiation markers, repression of these markers and myocardin was attenuated in SM22α-Cre/IκBΔN mice. Consistent with these findings, NF-κB activation by interleukin-1β (IL-1β) decreased expression of SMC differentiation markers as well as myocardin in cultured SMCs. Inhibition of NF-κB signaling by BAY 11-7082 attenuated repressive effects of IL-1β. Of interest, Krüppel-like factor 4 (Klf4), a transcription factor critical for regulating SMC differentiation and proliferation, was also involved in IL-1β-mediated myocardin repression. Promoter analyses and chromatin immunoprecipitation assays revealed that NF-κB repressed myocardin by binding to the myocardin promoter region in concert with Klf4.
conclusionsThese results provide novel evidence that activation of the NF-κB pathway cell-autonomously mediates SMC phenotypic switching and contributes to neointima formation following vascular injury.
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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.