ArticleInternational journal of surgery (London, England)2026
Selenomethionine alleviates aortic dissection via PGC-1α/NRF2/TFAM-mediated mitochondrial biosynthesis against ferroptosis: an experimental study.
Article in International journal of surgery (London, England), 2026. 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.
- Reactive oxygen species in thoracic aortic dissection: Insights into mechanisms and disease progression.Redox biology · 2026Review
- Bioinformatics Analysis of Ferroptosis-Related Driver Genes in Stanford Type A Aortic Dissection.Current issues in molecular biology · 2026Article
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7 authors.
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Abstract
backgroundAortic dissection (AD) is a cardiovascular disease with an extremely high mortality rate, and there is currently a lack of specific therapeutic drugs clinically. Selenomethionine (Set), known for its antioxidant and anti-inflammatory properties, has demonstrated promising potential in the treatment of cardiovascular diseases. Here, its therapeutic efficacy in AD and underlying mechanisms were explored.
methodsThe mouse model was established by β-aminopropionitrile fumarate induction. The effects of Set on aortic dilation, histopathology, and survival rate were evaluated. In vitro , platelet-derived growth factor-BB (PDGF-BB)-induced phenotypic switching of vascular smooth muscle cells (VSMCs) was utilized. EdU assay, Transwell migration assay, and lipid peroxidation experiments were conducted to analyze the impact of Set. Key molecular mechanisms were further validated through single-cell sequencing, transcriptomic analysis, and small interfering RNAs knockdown techniques.
resultsIn vivo experiments demonstrated that Set significantly reduced the incidence and mortality of AD, suppressed aortic dilation, alleviated elastic fiber fragmentation, and inhibited collagen hyperplasia. In vitro , Set effectively attenuated PDGF-BB-induced proliferation, migration, and phenotypic switching of VSMCs. Single-cell sequencing revealed marked enrichment of ferroptosis-related genes in VSMCs from patients with AD. Transcriptomic analysis indicated that Set substantially inhibited ferroptosis signaling and activated mitochondrial biogenesis pathways. Mechanistically, Set activated the PGC-1α/NRF2 pathway, upregulated GPX4 expression, reduced lipid peroxidation, and improved mitochondrial function, ultimately suppressing phenotypic switching of VSMCs. Notably, knockdown of GPX4 or PGC-1α weakened the inhibitory effects of Set on VSMCs' phenotypic switching.
conclusionsSet alleviated AD progression by suppressing ferroptosis-mediated phenotypic switching of VSMCs through targeted activation of the PGC-1α/NRF2/TFAM axis.
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