ArticleThe American journal of cardiology2012
Relation of cytosolic iron excess to cardiomyopathy of Friedreich's ataxia.
Article in The American journal of cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Serial assessment of echocardiographic measures in Friedreich ataxia.American heart journal plus : cardiology research and practice · 2026Article
- Pathological frataxin deficiency in mice causes tissue-specific alterations in iron homeostasis.iScience · 2026Article
- Long non-coding RNABrain communications · 2024Article
- Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Cerebral Iron Deposition in Neurodegeneration.Biomolecules · 2022Review
- Ectopic Burden via Holter Monitors in Friedreich Ataxia.Pediatric neurology · 2021Observational
- Friedreich cardiomyopathy is a desminopathy.Free neuropathology · 2021Article
- Molecular Defects in Friedreich's Ataxia: Convergence of Oxidative Stress and Cytoskeletal Abnormalities.Frontiers in molecular biosciences · 2020Review
- The Efficacy of Iron Chelators for Removing Iron from Specific Brain Regions and the Pituitary-Ironing out the Brain.Pharmaceuticals (Basel, Switzerland) · 2019Review
- The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.Frontiers in neuroscience · 2019Review
- Iron chelation by curcumin suppresses both curcumin-induced autophagy and cell death together with iron overload neoplastic transformation.Cell death discovery · 2019Article
- Role of frataxin protein deficiency and metabolic dysfunction in Friedreich ataxia, an autosomal recessive mitochondrial disease.Neuronal signaling · 2018Review
- Iron in Friedreich Ataxia: A Central Role in the Pathophysiology or an Epiphenomenon?Pharmaceuticals (Basel, Switzerland) · 2018Review
- Article
- Impact ofInternational journal of molecular sciences · 2018Review
- Balance of cardiac and systemic hepcidin and its role in heart physiology and pathology.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Review
- Nanoscopic X-ray fluorescence imaging and quantification of intracellular key-elements in cryofrozen Friedreich's ataxia fibroblasts.PloS one · 2018Article
- Needs and Requirements of Modern Biobanks on the Example of Dystonia Syndromes.Frontiers in neurology · 2017Article
- Liver Growth Factor (LGF) Upregulates Frataxin Protein Expression and Reduces Oxidative Stress in Friedreich's Ataxia Transgenic Mice.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiomyopathy is the leading cause of death in Friedreich's ataxia. This autosomal recessive disease is caused by a homozygous guanine-adenine-adenine trinucleotide repeat expansion in the frataxin gene (chromosome 9q21). One untoward effect of frataxin deficiency is the lack of iron (Fe)-sulfur clusters. Progressive remodeling of the heart in FA, however, may be more specifically related to sarcoplasmic Fe overload. The Fe-containing inclusions in a small percentage of cardiomyocytes may not represent purely mitochondrial accumulation of the metal. The objective of the present study was to re-examine the contribution of Fe to cardiomyocyte hypertrophy, fiber necrosis, and myocardial scarring, using a combination of X-ray fluorescence, slide histochemistry of Fe, and immunohistochemistry of 2 Fe-related proteins. Polyethylene glycol-embedded human cardiac tissues from the left and right ventricular walls, ventricular septum, right atrium, and atrial septum were studied using qualitative and quantitative X-ray fluorescence. Tissues were recovered from the polyethylene glycol matrix, re-embedded in paraffin, and sectioned for visualization of Fe, ferritin, and ferroportin. X-ray fluorescence showed quantifiable levels of Fe and zinc. Regions of significantly increased Fe (1 to 4 mm(2)) were irregularly distributed throughout the working myocardium. Fe granules were sparse in conductive tissue. Zinc signals remained unchanged. Robust cytosolic ferritin reaction product occurred in many fibers of the affected regions. Ferroportin displayed no response except in fibers with advanced Fe overload. These observations are at variance with the concept of selective Fe overload only in cardiac mitochondria. In conclusion, Fe-mediated damage to cardiomyocytes and myocardial scarring are more likely due to cytosolic Fe excess.
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Registered trials
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