ArticleRedox report : communications in free radical research2025
Melatonin inhibits ferroptosis in myocardial ischemia/reperfusion injury by inhibiting the ATM/p53 signaling pathway.
Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- The Interplay of Programmed Cell Death Networks in Cardiovascular Diseases: Mechanisms and Therapeutic Opportunities.Reviews in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMelatonin is a powerful free radical scavenger, with cardioprotective effects; however, the mechanism of this cardioprotective activity remains unclear. We hypothesized that melatonin inhibits ferroptosis and protects cardiomyocytes through suppression of the ataxia telangiectasia mutated (ATM)/p53 signaling pathway and reduction of lipid peroxidation.
methodsForty-two rat hearts were randomly assigned to a control group or one of six experimental groups (I/R, I/R + melatonin, I/R + melatonin + chloroquine diphosphate5, I/R + chloroquine diphosphate1, I/R + chloroquine diphosphate5, I/R + chloroquine diphosphate25). Thirty C57/BL6 male mice were assigned to 5 groups, with the same grouping as rats. The hearts were reperfused, after which the levels of creatine kinase MB, malondialdehyde, superoxide dismutase, iron, and glutathione/ glutathione oxidized were measured. Triphenyl tetrazolium chloride (TTC) staining, Hematoxylin and eosin staining, X-ray electron microscopy, western blotting, and immunofluorescence were performed to evaluate the effects of melatonin treatment on the pathology, microstructure, and antioxidant enzymes of the myocardium (ferritin heavy chain 1 (FTH1), SLC7A11 (XCT), superoxide dismutase-2 (SOD-2), and glutathione peroxidase 4 (GPX4), p53, and p-p53).
resultsIschemia/reperfusion increased myocardial lipid peroxidation, iron and p53 contents, as well as damage to the myocardial pathology and mitochondrial structure, and decreased the expression levels of antioxidant enzymes. Melatonin treatment alleviated these effects, which were reversed by chloroquine diphosphate.
conclusionsThese findings suggest that melatonin pretreatment protects cardiomyocytes from I/R injury by inhibiting cell ferroptosis via suppression of the ATM/p53 signaling pathway.
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.