ArticleChinese medicine2025
Magnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- DietaryJournal of microbiology and biotechnology · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation.Cell death discovery · 2026Review
- Correction: Magnolia kobus DC. suppresses neointimal hyperplasia by regulating ferroptosis and VSMC phenotypic switching in a carotid artery ligation mouse model.Chinese medicine · 2025Article
- The interplay of ferroptosis and oxidative stress in the pathogenesis of aortic dissection.Frontiers in pharmacology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
backgroundMagnolia kobus DC (MO), as a plant medicine, has been reported to have various physiological activities, including neuroprotective, anti-inflammatory, and anti-diabetic effects. However, vascular protective effects of MO remain incompletely understood. In this study, we evaluated the vascular protective effect of MO against ferroptosis in a carotid artery ligation (CAL)-induced neointimal hyperplasia mouse model and in aortic thoracic smooth muscle A7r5 cells.
methodsThis study was conducted to estimate the vascular protective effects of MO by systematically measuring histopathological analysis and western blot analysis in CAL animal model. In vitro protective effects of MO were evaluated by estimating cell viability, reactive oxygen species (ROS) content, glutathione (GSH) levels, lipid peroxidation, mitochondrial morphological change, cell proliferation, migration, western blot analysis, and qRT-PCR against erastin (Era)-induced A7r5 cells.
resultsMO intake significantly improved neointimal formation, inhibited ferroptosis and vascular smooth muscle cell (VSMC) phenotypes, and ameliorated the antioxidant system of carotid artery tissues. In addition, MO treatment effectively ameliorated Era-induced ferroptotic cytotoxicity, including cellular death, ROS production, and cell migration status. MO treatment also suppressed proliferation and migration in Era-induced A7r5 cells. MO considerably regulated Era-induced abnormal mechanisms related to ferroptotic changes, VSMC phenotype switching, and the ROS scavenging system in A7r5 cells.
conclusionMO has the potential for use as a functional food supplement, nutraceutical, or medicinal food, with protective effects on vascular health by regulating ferroptosis and VSMC phenotypic switching.
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