ArticleFrontiers in pharmacology2025
Salidroside can protect against ferroptosis in cardiomyocytes and may be related to the regulation of GGT1.
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 5 papers.
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Who cites it
5 citing papers in PubMed.
- Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated deubiquitination of PRDX2.International journal of molecular medicine · 2026Article
- Combining network pharmacology and experimental validation to demonstrate that salidroside alleviates acute lung injury by inhibiting ferroptosis via the MAPK/GPX4 pathway.Respiratory research · 2026Article
- Mechanistic Investigation of Salidroside Modulates Iron Overload to Mitigate Radiation-Induced Heart Disease.Cardiovascular therapeutics · 2026Article
- Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review.Drug design, development and therapy · 2026Review
- Salidroside and inflammation-linked disorders: integrative insights into the pharmacological effects and mechanistic targets.Inflammopharmacology · 2025Review
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Authors and funding
10 authors.
Funding
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Abstract
Indroduction: Ferroptosis, an iron-dependent cell death mechanism driven by lipid peroxidation, represents a novel therapeutic target for myocardial injury. Salidroside (SAL), a natural bioactive compound derived from Rhodiola rosea, exhibits cardioprotective effects through multi-target mechanisms with minimal adverse effects, yet its precise role in ferroptosis regulation remains unclear. Methods: This study systematically investigated SAL's anti-ferroptotic effects using Results: SAL treatment significantly enhanced cardiomyocyte viability by attenuating ferroptotic hallmarks, including lipid ROS accumulation, iron overload, lipid peroxidation, and mitochondrial dysfunction. Transcriptomic analysis revealed SAL-mediated modulation of DNA replication/repair, cell cycle regulation, protein autophosphorylation, drug ADME processes, and glutathione metabolism-a critical pathway in ferroptosis. Molecular docking identified γ-glutamyltransferase 1 (GGT1) as a high-affinity SAL target, linking drug metabolism and glutathione homeostasis. In MI mice, SAL downregulated GGT1 expression while restoring ferroptosis-related biomarkers: upregulating GPX4 and reducing SLC7A11/LC3II levels. Mechanistically, SAL suppresses ferroptosis through dual regulation of GGT1: (1) enhancing glutathione synthesis via GGT1 inhibition and (2) potentiating GPX4-mediated antioxidant defense. Discussion: These findings establish GGT1 as a pivotal therapeutic target for SAL's cardioprotection, providing a mechanistic basis for its clinical application in ferroptosis-associated cardiovascular diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.