ArticleJournal of pharmaceutical analysis2025
Ginger protects against vein graft remodeling by precisely modulating ferroptotic stress in vascular smooth muscle cell dedifferentiation.
Article in Journal of pharmaceutical analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- Ferroptosis of smooth muscle cells in vascular diseases: from basic principles to clinical translation.Cell death discovery · 2026Review
- CIAPIN1 functions as a redox-sensitive transcriptional repressor ofTheranostics · 2026Article
- Article
- Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026Review
- Injury and cyclic stretch induce vein graft failure: effective treatment with zinc oxide-loaded electrospun polycaprolactone external stent.Regenerative biomaterials · 2025Article
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
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Authors and funding
9 authors.
Funding
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Abstract
Vein graft (VG) failure (VGF) is associated with VG intimal hyperplasia, which is characterized by abnormal accumulation of vascular smooth muscle cells (VSMCs). Most neointimal VSMCs are derived from pre-existing VSMCs via a process of VSMC phenotypic transition, also known as dedifferentiation. There is increasing evidence to suggest that ginger or its bioactive ingredients may block VSMC dedifferentiation, exerting vasoprotective functions; however, the precise mechanisms have not been fully characterized. Therefore, we investigated the effect of ginger on VSMC phenotypic transition in VG remodeling after transplantation. Ginger significantly inhibited neointimal hyperplasia and promoted lumen (L) opening in a 3-month VG, which was primarily achieved by reducing ferroptotic stress. Ferroptotic stress is a pro-ferroptotic state. Contractile VSMCs did not die but instead gained a proliferative capacity and switched to the secretory type, forming neointima (NI) after vein transplantation. Ginger and its two main vasoprotective ingredients (6-gingerol and 6-shogaol) inhibit VSMC dedifferentiation by reducing ferroptotic stress. Network pharmacology analysis revealed that 6-gingerol inhibits ferroptotic stress by targeting P53, while 6-shogaol inhibits ferroptotic stress by targeting 5-lipoxygenase (Alox5), both promoting ferroptosis. Furthermore, both ingredients co-target peroxisome proliferator-activated receptor gamma (
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