ArticlePhysiological reports2025
Critical role of the β isoform of protein kinase C (PKCβ) in angiotensin II-induced oxidative stress in vascular smooth muscle cells.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Protective Effect of the NHE1 Inhibitor Buthutin A on Oxidative Stress-Induced Apoptosis in HUVECs.ACS omega · 2026Article
- [Untargeted metabolomics-based exploration of potential metabolic biomarkers for subclinical atherosclerosis in metabolic-associated fatty liver disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Critical role of the β isoform of protein kinase C (PKCβ) in angiotensin II-induced oxidative stress in vascular smooth muscle cells.Physiological reports · 2025Article
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11 authors.
Funding
Abstract
The aim of this study was to elucidate the role of protein kinase Cβ (PKCβ) in subacute angiotensin II (Ang II)-induced oxidative stress and the mechanism of its effects on vascular smooth muscle cells (VSMCs) using a PKCβ-knockout strategy. Both short-term (30 min) and prolonged (24 h) treatment with Ang II increased reactive oxygen species (ROS) production through NADPH oxidase (NOX) activation, with increased phosphorylation of PKCβ at active site Ser660 in rat primary VSMCs from mesenteric artery. The increases in ROS production and NOX activity were completely abolished in VSMCs of PKCβ-knockout rats, in which the absence of PKCβ mRNA expression was confirmed. Genomic and pharmacologic analyses indicated that prolonged treatment with Ang II increased ROS production via NF-κB-mediated NOX1 and p22
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