ArticleFrontiers in pharmacology2025
Pharmacological activation of SIRT1-AMPK by ginsenoside Rb1: a novel therapeutic strategy for pressure injury
Article in Frontiers in pharmacology, 2025. 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.
- Global hotspots and trends in AMPA receptor research (2000-2025): a bibliometric and visualization analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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7 authors.
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Abstract
Background: Pressure injuries (PIs) are a major clinical problem, and current treatments offer limited efficacy. Ferroptosis-driven oxidative damage and chronic inflammation severely impair wound healing. Ginsenoside Rb1 (Rb1), a bioactive component of Method: Transcriptomic profiling was performed on dorsal skin tissues from normal rats, pressure injury rats, and Rb1-treated rats using RNA sequencing to identify differentially expressed genes (DEGs), followed by Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, network pharmacology analysis, and protein-protein interaction (PPI) network construction to screen potential regulatory pathways. Results: Integrated transcriptomic and network pharmacology analyses identified the SIRT1-AMPK axis as a key mediator of Rb1-induced wound repair. Conclusion: Rb1 functions as an SIRT1-AMPK activator that inhibits ferroptosis and inflammation to promote PI wound healing. These findings underpin the efficacy of Rb1 as a promising multi-target therapeutic candidate for future clinical development.
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