ArticleExperimental and therapeutic medicine2026
Ginsenoside Re attenuates homocysteine-induced endothelial cell ferroptosis through upregulation of GPX4/xCT signaling.
Article in Experimental and therapeutic medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Ginsenosides: potential therapeutic implications in neurodegenerative diseases by inhibiting ferroptosis.Molecular biology reports · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction is a key pathophysiological basis of atherosclerosis (AS). Potential mechanisms by which Hcy causes vascular injury include inhibiting endothelial cell growth, inducing endothelial dysfunction, and promoting vascular remodeling. Suppression of GPX4 synthesis can lead to exacerbated lipid peroxidation, triggering ferroptosis. The objective of the present study was to investigate whether ginsenoside Re attenuates homocysteine (Hcy)-induced endothelial cell ferroptosis by upregulating glutathione peroxidase 4 (GPX4). After treating EA.hy926 cells with different concentrations of Hcy for 24 h, cell viability was assessed using an MTT assay to determine the appropriate concentrations of Hcy for establishing a cell damage model. EA.hy926 cells were then divided into the following four groups: Control group, Hcy group, low-dose ginsenoside Re + Hcy group and high-dose ginsenoside Re + Hcy group. Cell viability was assessed using an MTT assay, whereas the BODIPY
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