ArticleActa pharmacologica Sinica2025
Endothelial Gsα deficiency promotes ferroptosis and exacerbates atherosclerosis in apolipoprotein E-deficient mice via the inhibition of NRF2 signaling.
Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Single-cell RNA sequencing pseudobulk analysis and machine learning identify candidate biomarkers for ischemic cardiomyopathy.Frontiers in cardiovascular medicine · 2026Article
- Ferroptosis of Macrophages and Endothelial Cells in Atherosclerosis: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2025Review
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15 authors.
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Abstract
The importance of ferroptosis in the occurrence and progression of atherosclerosis is gradually being recognized. The stimulatory G protein α subunit (Gsα) plays a crucial role in the physiology of endothelial cells (ECs). Our previous study showed that endothelial Gsα could regulate angiogenesis and preserve endothelial permeability. In this study, we investigated whether endothelial Gsα contributed to atherosclerosis through ferroptosis and oxidative stress. We generated endothelial Gsα-specific knockout mice in apolipoprotein E-deficient (ApoE
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