ArticleRedox report : communications in free radical research2025
Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.
Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Psychological Stress and Male Infertility: Oxidative Stress as the Common Downstream Pathway.Biomedicines · 2026Review
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSympathetic overactivity is closely associated with vascular remodeling. Sympathetic fibers dominantly innervate the adventitia of arteries rather than tunica media. Vascular adventitial fibroblasts (VAFs) play crucial roles in vascular remodeling. However, the link between sympathetic overactivity and VAF proliferation and migration is unknown.
methodsPrimary VAFs were isolated from the thoracic aorta of spontaneously hypertensive rats and Wistar-Kyoto rats. Norepinephrine (NE) bitartrate monohydrate was applied to VAFs to simulate the sympathetic overactivity.
resultsNE increased NADPH oxidase (NOX) 2 expression and superoxide level, which were almost abolished by NOX2 inhibitor GSK2795039 or α-adrenoceptor antagonist prazosin, but not significantly affected by NOX1 inhibitor ML171, NOX4 inhibitor GLX351322 or β-adrenoceptor antagonist propranolol. Superoxide scavenger tempol or NOX2 inhibitor GSK2795039 attenuated NE-induced VAF proliferation and migration. NE promoted protein kinase C (PKC) phosphorylation and NFκB-p65 nuclear translocation. Either PKC inhibitor Go6983 or NFκB inhibitor BAY11-7082 attenuated NE-induced NOX activation, NOX2 upregulation, superoxide production, proliferation and migration.
conclusionNE promotes oxidative stress by α-receptor/PKC/NFκB-mediated NOX2 upregulation, which contributes to proliferation and migration of VAFs.
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Registered trials
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