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Apoptotic myocardial cell death in the setting of arrhytmogenic right ventricular cardiomyopathy
Abstract
BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary heart muscle disease characterized by progressive atrophy of the right ventricular myocardium accompanied by fibro-fatty replacement. We examined whether the loss of myocardial cells in the setting of ARVC could result from cell death by apoptosis as demonstrated by the detection of DNA fragmentation and the expression of apoptosis regulatory proteins (e.g. CPP-32, Bcl-2, and Bax). METHODS: Specimens obtained from the right ventricular myocardium of 11 patients with ARVC (ARVC group) and 10 age-matched normal individuals (control group) were analysed. To identify individual cells undergoing apoptosis, paraffin sections were examined with the TdT-mediated dUTP-biotin nick end labelling method (TUNEL) and the rabbit polyclonal anti-single stranded DNA method (ssDNA). The apoptotic index was calculated as the percentage of nuclei staining positive by the TUNEL or ssDNA method. We also used immunohistochemical techniques to examine the levels of CPP-32, Bcl-2, and Bax expression. RESULTS: Apoptosis was detected in the ARVC group with a mean apoptotic index of 5.7 +/- 4.5% (ssDNA) and 23.8 +/- 7.5% (TUNEL), but not in the control group (p < 0.01). CPP-32 expression and Bax overexpression were observed in the ARVC group. However, Bcl-2 expression was not seen in either group. CONCLUSIONS: Apoptotic myocardial cell death occurs in the setting of ARVC and may contribute to the loss of myocardial cells.
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“suggesting myocardial destruction may be episodic rather than a gradual loss.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [98]
In the citing paper
“Histopathological analyses using a variety of immunohistochemical techniques have demonstrated increased apoptotic cardiomyocyte death in ACM, with apoptotic indices reaching approximately 24% in early symptomatic patients [97,98], suggesting myocardial destruction may be episodic rather than a gradual loss.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [98]
In the citing paper
“Additional mitochondrial apoptotic markers include CPP-32 and BAX with absent BCL-2 expression [98].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [98]
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Metadata
- Authors
- YAMAJI, K., FUJIMOTO, S., IKEDA, Y., MASUDA, K., NAKAMURA, S., SAITO, Y., & YUTANI, C.
- Affiliations
- Nara Medical University (JP)
- Venue
- Acta Cardiologica
- Publisher
- Peeters Publishers
- Published
- 2005-11-01
- Volume
- 60
- Issue
- 5
- Pages
- 465-470
- ISSN
- 0001-5385 (ISSN-L)
- OpenAlex
- W1981800414
- Cited by
- 24
- References
- 0
- Citations by year
- 2026: 2 · 2025: 1 · 2023: 2 · 2021: 1 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 2
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Cardiologica (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- arrhythmogenic right ventricular cardiomyopathy, apoptosis, myocardial cell death, DNA fragmentation, Bax, Bcl-2, right ventricular myocardium, fibrofatty replacement, TUNEL
- MeSH terms
- Adult, Aged, Female, Heart Ventricles, Humans, Immunohistochemistry, Male, Middle Aged, Myocardium, Biomarkers, Cell Death, Apoptosis, Proto-Oncogene Proteins c-bcl-2, Arrhythmogenic Right Ventricular Dysplasia, Caspases, In Situ Nick-End Labeling, Myocytes, Cardiac, bcl-2-Associated X Protein, Caspase 3
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