ReviewHeart failure reviews2018
Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update.
Review in Heart failure reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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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.
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
62 citing papers in PubMed, 94 citations in OpenAlex.
- Trial
- Subcellular regulation of ferroptosis: roles of individual intracellular organelles and cross talk.American journal of physiology. Cell physiology · 2026Review
- Iron and Copper Homeostasis in Cardiometabolic Disease: Therapeutic Potential of Chelators.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Molecular and Cellular Determinants of Human Iron Overload Cardiomyopathy.bioRxiv : the preprint server for biology · 2026Article
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- Doxorubicin-induced cardiotoxicity: Is ferroptosis the primary driver or a downstream amplifier?EXCLI journal · 2026Review
- Acute kidney injury and iron metabolism: A narrative review focusing on pathophysiology and therapy.Smart molecules : open access · 2025Review
- Cardiac Magnetic Resonance Guidance for the Pathogenetic Definition of Cardiomyopathies.Current cardiology reports · 2025Review
- PINK1-deficiency facilitates mitochondrial iron accumulation and colon tumorigenesis.Autophagy · 2025Article
- Cardiac injury caused by iron overload in thalassemia.Frontiers in pediatrics · 2025Review
- Iron Metabolism in Cardiovascular Disease.Advances in experimental medicine and biology · 2025Review
- Ferroptosis: The Pivotal Link in Cardiovascular Diseases Pathogenesis and Therapy.International journal of general medicine · 2025Review
- The role of redox-active iron, copper, manganese, and redox-inactive zinc in toxicity, oxidative stress, and human diseases.EXCLI journal · 2025Review
- The role of mitochondria in iron overload-induced damage.Journal of translational medicine · 2024Review
- Targeting ferroptosis by natural products in pathophysiological conditions.Archives of toxicology · 2024Review
- Ferroptosis and its Potential Determinant Role in Myocardial Susceptibility to Ischemia/Reperfusion Injury in Diabetes.Reviews in cardiovascular medicine · 2024Review
- Ferroptosis contributing to cardiomyocyte injury induced by silica nanoparticles via miR-125b-2-3p/HO-1 signaling.Particle and fibre toxicology · 2024Article
- The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024Review
- The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024Review
- Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Iron overload cardiomyopathy (IOC) is a major cause of death in patients with diseases associated with chronic anemia such as thalassemia or sickle cell disease after chronic blood transfusions. Associated with iron overload conditions, there is excess free iron that enters cardiomyocytes through both L- and T-type calcium channels thereby resulting in increased reactive oxygen species being generated via Haber-Weiss and Fenton reactions. It is thought that an increase in reactive oxygen species contributes to high morbidity and mortality rates. Recent studies have, however, suggested that it is iron overload in mitochondria that contributes to cellular oxidative stress, mitochondrial damage, cardiac arrhythmias, as well as the development of cardiomyopathy. Iron chelators, antioxidants, and/or calcium channel blockers have been demonstrated to prevent and ameliorate cardiac dysfunction in animal models as well as in patients suffering from cardiac iron overload. Hence, either a mono-therapy or combination therapies with any of the aforementioned agents may serve as a novel treatment in iron-overload patients in the near future. In the present article, we review the mechanisms of cytosolic and/or mitochondrial iron load in the heart which may contribute synergistically or independently to the development of iron-associated cardiomyopathy. We also review available as well as potential future novel treatments.
Indexed as
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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.