ArticleEuropean journal of medical research2025
Low doses of ozone alleviate cardiomyocyte ferroptosis induced by hypoxia-reoxygenation injury via the AMPK-mTOR pathway.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Total Flavonoids ofNutrients · 2026Article
- Angelica sinensis polysaccharide nanoparticles can improve myocardial ischemia-reperfusion injury by inhibiting ferritinophagy via the ATF6/NCOA4 pathway.Journal of translational medicine · 2026Article
- Iron-dependent ferroptosis in cardiac microvascular endothelial cells: a key link between dysregulated iron homeostasis and microcirculatory injury during myocardial ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Review
- Anisotropic Micro/Nanotopography Regulating Mitochondrial Dynamics in Cardiomyocytes.Research (Washington, D.C.) · 2025Article
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2 authors.
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Abstract
backgroundAcute myocardial infarction (AMI), a sudden and dangerous form of cardiovascular diseases (CVDs), induces myocardial hypoxia-reoxygenation (H/R) injury, which exacerbates myocardial damage and potentially results in heart failure. In this study, we explored the effect of low-concentration ozone after hypoxia-reoxygenation injury.
methodsCCK-8 assay and flow cytometry wisere performed to assess cell viability. To evaluate ferroptosis, ferroptosis-related protein expression levels, intracellular Fe
resultsThe results discovered that an appropriate dose of ozone can effectively mitigate ferroptosis in H9c2 cardiomyocytes induced by hypoxia-reoxygenation. Erastin successfully antagonized the effects of ozone, further confirming ozone's significant role in regulating ferroptosis. Mechanistically, ozone effectively suppressed intracellular oxidative stress levels, thereby activating the AMPK-mTOR pathway. In addition, dorsomorphin successfully blocked the effects of ozone and exacerbated ferroptosis following hypoxia-reoxygenation, suggesting the regulation of AMPK-mTOR pathway.
conclusionsLow-concentration ozone treatment has shown promise in mitigating ferroptosis by regulating the AMPK-mTOR pathway, highlighting its potential as a therapeutic agent for hypoxia-reoxygenation injury.
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