ArticleRedox report : communications in free radical research2024
Melittin alleviates sepsis-induced acute kidney injury by promoting GPX4 expression to inhibit ferroptosis.
Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Research landscape and emerging themes of ferroptosis in sepsis-associated acute kidney injury: a bibliometric and science-mapping analysis (2016-2025).Frontiers in pharmacology · 2026Pooled it
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Rhapontigenin Alleviates Sepsis-Associated Acute Kidney Injury and Is Accompanied by Modulation of Ferroptosis, Inflammation, and NF-κB Signaling.Journal of biochemical and molecular toxicology · 2026Article
- Inhibition of EphA2 triggers ferroptosis by disrupting USP38mediated SLC7A11 stabilization in chemoresistant gastric cancer.Cellular and molecular life sciences : CMLS · 2026Article
- From Toxin to Therapy: Biomedical Applications of Bee Venom in Cancer, Diabetes, and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Magnolol Ameliorates Cisplatin-Induced Acute Kidney Injury with Activation of Nrf2-Associated Antioxidant Responses.Current issues in molecular biology · 2026Article
- M1 macrophage exosomes induce ferroptosis via MiR-582-5p-mediated ZBTB10 suppression in sepsis-induced acute kidney injury.Archives of medical science : AMS · 2026Article
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Cinnamaldehyde attenuates LPS-induced acute kidney injury by inhibiting ferroptosis via the Gsk3β/Nrf2/Gpx4 pathway.American journal of translational research · 2026Article
- Protective effects and mechanisms of cynaroside on renal fibrosis in mice with unilateral ureteral obstruction.Redox report : communications in free radical research · 2025Article
- Melittin Nanoparticles Mitigate Glyphosate-Induced Nephrotoxicity via Cytokine Modulation and Bax/Nrf2 Pathways.Biomedicines · 2025Article
- Therapeutic Bioactivity Exerted by theMolecules (Basel, Switzerland) · 2025Article
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Ferroptosis mediated by the IDO1/Kyn/AhR pathway triggers acute thymic involution in sepsis.Cell death & disease · 2025Article
- Pharmacological inhibition of STING-mediated GPX4 autophagic degradation by 4-octyl itaconate ameliorates sepsis-induced acute kidney injury.Apoptosis : an international journal on programmed cell death · 2025Article
- Article
- Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025Review
- Review of research progress in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesMelittin, the main component of bee venom, is a natural anti-inflammatory substance, in addition to its ability to fight cancer, antiviral, and useful in diabetes treatment. This study seeks to determine whether melittin can protect renal tissue from sepsis-induced damage by preventing ferroptosis and explore the protective mechanism.
methodsIn this study, we investigated the specific protective mechanism of melittin against sepsis-induced renal injury by screening renal injury indicators and ferroptosis -related molecules and markers in animal and cellular models of sepsis.
resultsOur results showed that treatment with melittin attenuated the pathological changes in mice with lipopolysaccharide-induced acute kidney injury. Additionally, we found that melittin attenuated ferroptosis in kidney tissue by enhancing GPX4 expression, which ultimately led to the reduction of kidney tissue injury. Furthermore, we observed that melittin enhanced NRF2 nuclear translocation, which consequently upregulated GPX4 expression. our findings suggest that melittin may be a potential therapeutic agent for the treatment of sepsis-associated acute kidney injury by inhibiting ferroptosis through the GPX4/NRF2 pathway.
conclusionsOur study reveals the protective mechanism of melittin in septic kidney injury and provides a new therapeutic direction for Sepsis-AKI.
Indexed as
Identifiers
What OpenQuestion holds
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.