ArticleAdvances in redox research2026
Inhibition of smooth muscle phenotypic modulation by bardoxolone methyl, omaveloxolone, and cinnamaldehyde is Nrf-2 dependent.
Article in Advances in redox research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neointimal hyperplasia (NH) is a primary cause of arterial restenosis following angioplasty, driven by oxidative stress and vascular smooth muscle cell (VSMC) phenotypic modulation. This study investigated whether the class I electrophilic Nrf2 activators Bardoxolone methyl (BAR), Omaveloxolone (OMV), and Cinnamaldehyde (CA) could suppress NH through Nrf2-dependent mechanisms. Using VSCM that were Nrf2 wild-type (WT), knockout (KO), and rescued by nrf2 lentiviral transduction, we assessed the effects of these activators on PDGF-induced proliferation, migration, and phenotypic modulation. Additionally, we utilized a rat carotid artery balloon injury model with periadventitial drug delivery and light-sheet fluorescence microscopy to evaluate neointimal formation.
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