ArticleHistology and histopathology2020
Microvascular pathology in Friedreich cardiomyopathy.
Article in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Ataxias: Hereditary, Acquired, and Reversible Etiologies.Seminars in neurology · 2023Article
- TGFβ signaling pathways in human health and disease.Frontiers in molecular biosciences · 2023Review
- Cardiovascular Research in Friedreich Ataxia: Unmet Needs and Opportunities.JACC. Basic to translational science · 2022Review
- Myocardial Perfusion Reserve in Children with Friedreich Ataxia.Pediatric cardiology · 2021Article
- Friedreich cardiomyopathy is a desminopathy.Free neuropathology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Heart disease is an integral part of Friedreich ataxia (FA). In addition to cardiomyocyte hypertrophy, fiber necrosis, and inflammatory infiltration, sections show fibrosis and disorganized capillaries. We examined the left ventricular wall (LVW) of 41 homozygous and 2 compound heterozygous FA patients aged 10-87 and 21 controls aged 2-69. Immunohistochemistry with an antibody to CD34 allowed quantitative counts of capillary profiles for a comparison with cardiomyocyte counts in the same field. Capillary counts (mean±standard deviation [SD]) in normal controls were 1926±341/mm², while mean cardiomyocyte counts were 2003±686/mm². The median ratio of capillaries to cardiomyocytes was 1.0 (interquartile range [IQR]: 0.9-1.2). In FA, the number of cardiomyocytes/mm² was significantly less (704±361; p<0.001), and the median ratio of capillaries to heart fibers was 2.0 (IQR:1.4-2.4). There was a significant correlation of the expanded guanine-adenine-adenine trinucleotides (shorter allele, GAA1) with a younger age of onset, shorter disease duration, and lower cardiomyocyte counts. The ratio of capillaries to heart fibers was higher in patients with long GAA1 repeat expansions (e.g., 3.31 in GAA1 of 1200). Double-label immunofluorescence for CD34 and the fibroblast marker S100A4 revealed co-expression in endothelial cells, supporting endothelial-to-mesenchymal transition in the pathogenesis of cardiac fibrosis in FA. We propose that the pathogenesis of FA heart disease includes primary fibrosis.
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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.