ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Melatonin mitigates the lipopolysaccharide-induced myocardial injury in rats by blocking the p53/xCT pathway-mediated ferroptosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
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Who cites it
7 citing papers in PubMed.
- Diquat-induced organ toxicity: a focus on regulated cell death pathways and mitochondrial dysfunction.Frontiers in cell and developmental biology · 2026Review
- Progress on Potential Therapeutic Targets for Sepsis-Related Cardiac Dysfunction: From Basic Research to Clinical Translation.ImmunoTargets and therapy · 2026Review
- Melatonin inhibits ferroptosis in myocardial ischemia/reperfusion injury by inhibiting the ATM/p53 signaling pathway.Redox report : communications in free radical research · 2025Article
- Review
- The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study.Journal of inflammation research · 2025Review
- Hydroxysafflor Yellow A Mitigates Sepsis-Induced Pulmonary and Intestinal Injury by Inhibiting TP53 Mediated Ferroptosis.Infection and drug resistance · 2025Article
- Melatonin Activates KEAP1/NRF2/PTGS2 Pathway to Attenuate Hyperoxia-Driven Ferroptosis in Bronchopulmonary Dysplasia.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This article examined the therapeutic effect of melatonin (MT) on the lipopolysaccharide (LPS)-induced myocardial injury, and the mechanisms involved. Septic rat model was constructed by exposing to lipopolysaccharide (LPS), and treated by MT, Ferrostatin-1 (Fer-1) and Erastin (Era). Hematoxylin-eosin staining was executed to appraise myocardial injury. H9c2 cells that exposed to LPS to induce in vitro sepsis cell model were treated by MT. p53 overexpression vectors were transfected into H9c2 cells. Inflammation- and ferroptosis-related indicators were examined by enzyme-linked immunosorbent assay. Expression of p53, xCT and GPX4 was scrutinized by quantitative real-time polymerase chain reaction and Western blot. MT relieved myocardial injury in septic rats. It decreased IL-6 and TNF-α, elevated GPX4 and GSH, and reduced MDA and Fe
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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.