ArticleProgress in pediatric cardiology2011
The Heart in Friedreich's Ataxia: Basic Findings and Clinical Implications.
Article in Progress in pediatric cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 33 citations in OpenAlex.
- Mitochondrial iron overload is associated with lysosomal dysfunction-mediated mitophagy impairment in the heart of Friedreich's ataxia.Mitochondrion · 2026Article
- AAV8 gene therapy reverses cardiac pathology and prevents early mortality in a mouse model of Friedreich's ataxia.Molecular therapy. Methods & clinical development · 2024Article
- Mitochondrial Iron Metabolism: The Crucial Actors in Diseases.Molecules (Basel, Switzerland) · 2022Review
- Friedreich ataxia: clinical features and new developments.Neurodegenerative disease management · 2022Review
- Fabry Disease Cardiomyopathy: A Review of the Role of Cardiac Imaging from Diagnosis to Treatment.Reviews in cardiovascular medicine · 2022Review
- Role of Iron-Related Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- Frataxin deficiency promotes endothelial senescence in pulmonary hypertension.The Journal of clinical investigation · 2021Article
- Hereditary muscle diseases and the heart: the cardiologist's perspective.European heart journal supplements : journal of the European Society of Cardiology · 2020Article
- Involvement of cytosolic and mitochondrial iron in iron overload cardiomyopathy: an update.Heart failure reviews · 2018Review
- Calcium Deregulation: Novel Insights to Understand Friedreich's Ataxia Pathophysiology.Frontiers in cellular neuroscience · 2018Article
- Mössbauer Spectra of Mouse Hearts Reveal Age-dependent Changes in Mitochondrial and Ferritin Iron Levels.The Journal of biological chemistry · 2017Article
- Increased Heme Levels in the Heart Lead to Exacerbated Ischemic Injury.Journal of the American Heart Association · 2015Article
- Iron-induced damage in cardiomyopathy: oxidative-dependent and independent mechanisms.Oxidative medicine and cellular longevity · 2015Review
- Modeling of Friedreich ataxia-related iron overloading cardiomyopathy using patient-specific-induced pluripotent stem cells.Pflugers Archiv : European journal of physiology · 2014Article
- Heme levels are increased in human failing hearts.Journal of the American College of Cardiology · 2013Article
- Mitochondria as a therapeutic target in heart failure.Journal of the American College of Cardiology · 2013Review
- Transition metals and mitochondrial metabolism in the heart.Journal of molecular and cellular cardiology · 2013Review
- Cardiac involvement in hereditary ataxias.Journal of child neurology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Friedreich's Ataxia is the most common inherited ataxia in man. It is a mitochondrial disease caused by severely reduced expression of the iron binding protein, frataxin. A large GAA triplet expansion in the human FRDA gene encoding this protein inhibits expression of this gene. It is inherited in an autosomal recessive pattern and typically diagnosed in childhood. The primary symptoms include severe and progressive neuropathy, and a hypertrophic cardiomyopathy that may cause death. The cardiomyopathy is difficult to treat and is frequently associated with arrhythmias, heart failure, and intolerance of cardiovascular stress, such as surgeries. Innovative approaches to therapy, such as histone deacetylase inhibitors, and enzyme replacement with cell penetrant peptide fusion proteins, hold promise for this and other similar mitochondrial disorders. This review will focus on the basic findings of this disease, and the cardiomyopathy associated with its diagnosis.
Identifiers
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.