ArticleCurrent medicinal chemistry2024
Ginsenoside Rg1 Suppresses Ferroptosis of Renal Tubular Epithelial Cells in Sepsis-induced Acute Kidney Injury
Article in Current medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 32 citations in OpenAlex.
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Ginsenosides: potential therapeutic implications in neurodegenerative diseases by inhibiting ferroptosis.Molecular biology reports · 2026Review
- Total Flavonoids of Rhizoma Drynariae Ameliorate Tendon-Bone Healing Following Anterior Cruciate Ligament Reconstruction in Rats by Activating the FSP1/CoQApplied biochemistry and biotechnology · 2026Article
- Emerging Role of Ferroptosis in Diabetes and Associated Complications: When Metabolic Dysregulation Meets Cell Death.Cell proliferation · 2026Review
- Ginsenoside-Mediated Ferroptosis Regulation: Bidirectional Effects and Therapeutic Potential in Diseases.International journal of molecular sciences · 2026Review
- Research progress on the regulation of ferroptosis in NPC (Review).Oncology reports · 2026Review
- Natural products reshape osteosarcoma cell fate: promoting cell death.Frontiers in pharmacology · 2026Review
- Research Progress on the Mechanism of Ginsenoside Rg1 in Inflammatory Bowel Disease.Journal of immunology research · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Ferroptosis, a Distinct Form of Cell Death, and Research Progress on Its Modulators.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Ferroptosis: molecular mechanisms, pathophysiology, and role in pediatric pulmonary diseases.Cell biology and toxicology · 2025Review
- Molecular Basis of Oxidative Stress-Induced Acute Kidney Injury, Kidney Fibrosis, Chronic Kidney Disease, and Clinical Significance of Targeting Reactive Oxygen Species-Regulated Pathways to Treat Kidney Disease.Frontiers in bioscience (Scholar edition) · 2025Review
- Ferroptosis: A key regulator and potential target for tissue injury.Histology and histopathology · 2025Review
- SIRT5-mediated HOXA5 desuccinylation inhibits ferroptosis to alleviate sepsis induced-lung injury.The Kaohsiung journal of medical sciences · 2025Article
- Advances in ginsenoside treatment for common kidney diseases: pharmacological evaluation and potential mechanisms.Frontiers in pharmacology · 2025Review
- Unraveling Ferroptosis: A New Frontier in Combating Renal Fibrosis and CKD Progression.Biology · 2024Review
- Metal-Dependent Cell Death in Renal Fibrosis: Now and in the Future.International journal of molecular sciences · 2024Review
- Observational
- Emerging insights into ferroptosis in cholangiocarcinoma (Review).Oncology letters · 2024Review
- Dexmedetomidine inhibits ferroptosis and attenuates sepsis-induced acute kidney injury via activating the Nrf2/SLC7A11/FSP1/CoQ10 pathway.Redox report : communications in free radical research · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSepsis-induced acute kidney injury is related to an increased mortality rate by modulating ferroptosis through ginsenoside Rg1. In this study, we explored the specific mechanism of it.
methodsHuman renal tubular epithelial cells (HK-2) were transfected with oe-ferroptosis suppressor protein 1 and treated with lipopolysaccharide for ferroptosis induction, and they were then treated with ginsenoside Rg1 and ferroptosis suppressor protein 1 inhibitor. Ferroptosis suppressor protein 1, CoQ
resultsLPS treatment diminished ferroptosis suppressor protein 1, CoQ
conclusionGinsenoside Rg1 alleviated sepsis-induced acute kidney injury by blocking renal tubular epithelial cell ferroptosis
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Registered trials
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 OpenQuestion graph.