ArticleInternational journal of molecular sciences2022
Counteraction of Myocardial Ferritin Heavy Chain Deficiency by Heme Oxygenase-1.
Article in International journal of molecular sciences, 2022. 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, 36 citations in OpenAlex.
- Article
- Phase-dependent iron dysmetabolism in myocardial ischemia-reperfusion injury: From mechanisms to therapies.American heart journal plus : cardiology research and practice · 2025Review
- IL-22 attenuates MAFLD progression by modulating oxidative stress and ferroptosis.Scientific reports · 2025Article
- Mitochondrial Ferritin Overexpression Attenuates Ferroptosis and Mitochondrial Dysfunction by Reducing VDAC1 to Relieve MI/RI-Induced Damage.Journal of cellular and molecular medicine · 2025Article
- Angiotensin type 1 and type 2 receptors-induced mitochondrial dysfunction promotes ferroptosis in cardiomyocytes.Journal of human hypertension · 2025Article
- Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.Frontiers in cardiovascular medicine · 2025Review
- Role of autophagy and ferroptosis in the development of endometriotic cysts (Review).International journal of molecular medicine · 2024Review
- [Research progress on the mechanism of action of heme oxygenase-1 regulating ferroptosis in non-alcoholic fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Review
- Ferrostatin-1 Blunts Right Ventricular Hypertrophy and Dysfunction in Pulmonary Arterial Hypertension by Suppressing the HMOX1/GSH Signaling.Journal of cardiovascular translational research · 2024Article
- Adipose knockout of H-ferritin improves energy metabolism in mice.Molecular metabolism · 2024Article
- Article
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- The Mechanisms of Ferroptosis Under Hypoxia.Cellular and molecular neurobiology · 2023Review
- Development and Validation of Robust Ferroptosis-Related Genes in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Article
- Heme oxygenase 1 alleviates nonalcoholic steatohepatitis by suppressing hepatic ferroptosis.Lipids in health and disease · 2023Article
- Ferritin heavy chain participated in ameliorating 3-nitropropionic acid-induced oxidative stress and apoptosis of goose follicular granulosa cells.Poultry science · 2023Article
- Review
- Current progress of ferroptosis in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Inflammation, dysregulated iron metabolism, and cardiovascular disease.Frontiers in aging · 2023Review
- Targeting ferroptosis as a promising therapeutic strategy to treat cardiomyopathy.Frontiers in pharmacology · 2023Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Given the abundance of heme proteins (cytochromes) in the mitochondrion, it is evident that a meticulously orchestrated iron metabolism is essential for cardiac health. Here, we examined the functional significance of myocardial ferritin heavy chain (FtH) in a model of acute myocardial infarction. We report that FtH deletion did not alter either the mitochondrial regulatory and surveillance pathways (fission and fusion) or mitochondrial bioenergetics in response to injury. Furthermore, deletion of myocardial FtH did not affect cardiac function, assessed by measurement of left ventricular ejection fraction, on days 1, 7, and 21 post injury. To identify the modulated pathways providing cardiomyocyte protection coincident with FtH deletion, we performed unbiased transcriptomic analysis. We found that following injury, FtH deletion was associated with upregulation of several genes with anti-ferroptotic properties, including heme oxygenase-1 (HO-1) and the cystine/glutamate anti-porter (Slc7a11). These results suggested that HO-1 overexpression mitigates ferroptosis via upregulation of Slc7a11. Indeed, using transgenic mice with HO-1 overexpression, we demonstrate that overexpressed HO-1 is coupled with increased Slc7a11 expression. In conclusion, we demonstrate that following injury, myocardial FtH deletion leads to a compensatory upregulation in a number of anti-ferroptotic genes, including HO-1. Such HO-1 induction leads to overexpression of Slc7a11 and protects the heart against ischemia-reperfusion-mediated ferroptosis, preserves mitochondrial function, and overall function of the myocardium.
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