ArticleBiomolecules2024
Exogenous Iron Induces Mitochondrial Lipid Peroxidation, Lipofuscin Accumulation, and Ferroptosis in H9c2 Cardiomyocytes.
Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2026Review
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2026Review
- Environmental Factors Drive Neurodegenerative Diseases Through Glutamate Excitotoxicity: A Convergent Mechanistic Pathway.Neuroscience bulletin · 2026Review
- Non-Erythropoietic EPO (EPO-R76E) Protects RPE Cells from Ferroptosis by Modulating the Labile Iron Pool and NRF2-GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- Protective role of sodium propionate against glycerol or fractionated doses of gamma rays-induced acute kidney injury via ATF5-induced mitophagy in rats.Scientific reports · 2026Article
- Piezo1 activation in endothelial cells aggravates microvascular ischemia-reperfusion injury in limbs by enhancing ferroptosis.Experimental & molecular medicine · 2026Article
- Resolving the cellular profile of germinal center-analogous microstructures in zebrafish.Frontiers in immunology · 2026Article
- Molecular mechanism and potential role of mitophagy in breast cancer.Journal of Cancer · 2026Review
- Lipofuscin accumulation in aging and neurodegeneration: a potential "timebomb" overlooked in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Article
- sPLA2-IIA modifies progranulin deficiency phenotypes in mouse models.Molecular neurodegeneration · 2025Article
- Integrated bioinformatics and experiment validation reveal cuproptosis-related biomarkers and therapeutic targets in sepsis-induced myocardial dysfunction.BMC infectious diseases · 2025Article
- Polydatin and Nicotinamide Prevent Iron Accumulation and Lipid Peroxidation in Cellular Models of Mitochondrial Diseases.Antioxidants (Basel, Switzerland) · 2025Article
- Ferroptosis: Mechanisms, Comparison with Cuproptosis and Emerging Horizons in Therapeutics.Oncology research · 2025Review
- Targeting ferroptosis: a promising avenue for ovarian cancer treatment.Frontiers in immunology · 2025Review
- Infantile neuroaxonal dystrophy: Molecular mechanisms and pathogenesis of PLA2G6-associated neurodegeneration.AIMS neuroscience · 2025Review
- Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025Review
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
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Authors and funding
6 authors.
Funding
Abstract
Lipid peroxidation plays an important role in various pathologies and aging, at least partially mediated by ferroptosis. The role of mitochondrial lipid peroxidation during ferroptosis remains poorly understood. We show that supplementation of exogenous iron in the form of ferric ammonium citrate at submillimolar doses induces production of reactive oxygen species (ROS) and lipid peroxidation in mitochondria that precede ferroptosis in H9c2 cardiomyocytes. The mitochondria-targeted antioxidant SkQ1 and the redox mediator methylene blue, which inhibits the production of ROS in complex I of the mitochondrial electron transport chain, prevent both mitochondrial lipid peroxidation and ferroptosis. SkQ1 and methylene blue also prevented accumulation of lipofuscin observed after 24 h incubation of cardiomyocytes with ferric ammonium citrate. Using isolated cardiac mitochondria as an in vitro ferroptosis model, it was shown that rotenone (complex I inhibitor) in the presence of ferrous iron stimulates lipid peroxidation and lipofuscin accumulation. Our data indicate that ROS generated in complex I stimulate mitochondrial lipid peroxidation, lipofuscin accumulation, and ferroptosis induced by exogenous iron.
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