ArticleJournal of molecular medicine (Berlin, Germany)2014
Mice lacking mitochondrial ferritin are more sensitive to doxorubicin-mediated cardiotoxicity.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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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.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Mitochondrial Ferritin in Subclinical Anthracycline-Induced Cardiotoxicity in Humans: A Pilot Study.Journal of cardiovascular translational research · 2026Article
- The regulation of mitochondrial ferritin on mitochondrial redox balance is essential to cell fate decision.Redox biology · 2026Review
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Gallic acid attenuates diabetic cardiomyopathy by inhibiting ferroptosis and protecting mitochondria via the TSPO/FTMT pathway.Frontiers in pharmacology · 2025Article
- A Brief History of Ferritin, an Ancient and Versatile Protein.International journal of molecular sciences · 2024Review
- Licochalcone A alleviates ferroptosis in doxorubicin-induced cardiotoxicity via the PI3K/AKT/MDM2/p53 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Molecular Mechanisms and Therapeutic Targeting of Ferroptosis in Doxorubicin-Induced Cardiotoxicity.JACC. Basic to translational science · 2024Review
- Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024Review
- Ferroptosis in diabetic cardiomyopathy: from its mechanisms to therapeutic strategies.Frontiers in endocrinology · 2024Review
- RNA mJACC. Basic to translational science · 2023Article
- Review
- The sGC-cGMP Signaling Pathway as a Potential Therapeutic Target in Doxorubicin-Induced Heart Failure: A Narrative Review.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Review
- Therapeutic Targets for DOX-Induced Cardiomyopathy: Role of Apoptosis vs. Ferroptosis.International journal of molecular sciences · 2022Review
- Understanding Anthracycline Cardiotoxicity From Mitochondrial Aspect.Frontiers in pharmacology · 2022Review
- Relevance of Ferroptosis to Cardiotoxicity Caused by Anthracyclines: Mechanisms to Target Treatments.Frontiers in cardiovascular medicine · 2022Review
- Role of Iron-Related Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- Understanding the Protective Role of Exosomes in Doxorubicin-Induced Cardiotoxicity.Oxidative medicine and cellular longevity · 2022Review
- Review
- Neurohormonal activation induces intracellular iron deficiency and mitochondrial dysfunction in cardiac cells.Cell & bioscience · 2021Article
- Regulated cell death pathways in doxorubicin-induced cardiotoxicity.Cell death & disease · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledMitochondrial ferritin is a functional ferritin that localizes in the mitochondria. It is expressed in the testis, heart, brain, and cells with active respiratory activity. Its overexpression in cultured cells protected against oxidative damage and reduced cytosolic iron availability. However, no overt phenotype was described in mice with inactivation of the FtMt gene. Here, we used the doxorubicin model of cardiac injury in a novel strain of FtMt-null mice to investigate the antioxidant role of FtMt. These mice did not show any evident phenotype, but after acute treatment to doxorubicin, they showed enhanced mortality and altered heart morphology with fibril disorganization and severe mitochondrial damage. Signs of mitochondrial damage were present also in mock-treated FtMt(-/-) mice. The hearts of saline- and doxorubicin-treated FtMt(-/-) mice had higher thiobarbituric acid reactive substance levels, heme oxygenase 1 expression, and protein oxidation, but did not differ from FtMt(+/+) in the cardiac damage marker B-type natriuretic peptide (BNP), ATP levels, and apoptosis. However, the autophagy marker LC3 was activated. The results show that the absence of FtMt, which is highly expressed in the heart, increases the sensitivity of heart mitochondria to the toxicity of doxorubicin. This study represents the first in vivo evidence of the antioxidant role of FtMt. KEY MESSAGE: Mitochondrial ferritin (FtMt) expressed in the heart has a protective antioxidant role. Acute treatment with doxorubicin caused the death of all FtMt(-/-) and only of 60 % FtMt(+/+) mice. The hearts of FtMt(-/-) mice showed fibril disorganization and mitochondrial damage. Markers of oxidative damage and autophagy were increased in FtMt(-/-) hearts. This is the first in vivo evidence of the antioxidant role of FtMt.
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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.