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Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy.

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Circulation research 📖 저널 OA 65.3% 2021: 3/3 OA 2022: 2/3 OA 2023: 4/8 OA 2024: 8/12 OA 2025: 14/24 OA 2026: 19/29 OA 2021~2026 2001 Vol.89(3) p. 279-86 cited 390 OA RCR 6.92 Viral Infections and Immunology Rese
TL;DR Cardiac cell death precedes ventricular decompensation and correlates with the time-dependent deterioration of function in this model, indicating that oxidative stress may be critical for activation of apoptosis in the overloaded heart.
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PubMed DOI OpenAlex Semantic 마지막 보강 2026-05-20
연도별 인용 (2012–2026) · 합계 187
OpenAlex 토픽 · Viral Infections and Immunology Research Cardiac electrophysiology and arrhythmias Cardiac Fibrosis and Remodeling

Cesselli D, Jakoniuk I, Barlucchi L, Beltrami AP, Hintze TH, Nadal-Ginard B

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Abstract

Cell death has been questioned as a mechanism of ventricular failure. In this report, we tested the hypothesis that apoptotic death of myocytes, endothelial cells, and fibroblasts is implicated in the development of the dilated myopathy induced by ventricular pacing. Accumulation of reactive oxygen products such as nitrotyrosine, potentiation of the oxidative stress response by p66(shc) expression, formation of p53 fragments, release of cytochrome c, and caspase activation were examined to establish whether these events were coupled with apoptotic cell death in the paced dog heart. Myocyte, endothelial cell, and fibroblast apoptosis was detected before indices of severe impairment of cardiac function became apparent. Cell death increased with the duration of pacing, and myocyte death exceeded endothelial cell and fibroblast death throughout. Nitrotyrosine formation and p66(shc) levels progressively increased with pacing and were associated with cell apoptosis. Similarly, p50 (DeltaN) fragments augmented paralleling the degree of cell death in the failing heart. Moreover, cytochrome c release and activation of caspase-9 and -3 increased from 1 to 4 weeks of pacing. In conclusion, cardiac cell death precedes ventricular decompensation and correlates with the time-dependent deterioration of function in this model. Oxidative stress may be critical for activation of apoptosis in the overloaded heart.
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Cardiac cell death precedes ventricular decompensation and correlates with the time-dependent deterioration of function in this model, indicating that oxidative stress may be critical for activation o

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APA 7 Cesselli, D., Jakoniuk, I., Barlucchi, L., Beltrami, A. P., Hintze, T. H., Nadal-Ginard, B., Kajstura, J., Leri, A., & Anversa, P. (2001). Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy.. Circulation research, 89(3), 279-86. https://doi.org/10.1161/hh1501.094115
Vancouver Cesselli D, Jakoniuk I, Barlucchi L, Beltrami AP, Hintze TH, Nadal-Ginard B, et al. Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy. Circulation research. 2001;89(3):279-86. doi:10.1161/hh1501.094115
AMA 11 Cesselli D, Jakoniuk I, Barlucchi L, Beltrami AP, Hintze TH, Nadal-Ginard B, et al. Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy. Circulation research. 2001;89(3):279-86. doi:10.1161/hh1501.094115
Chicago Cesselli, D., Jakoniuk, I., Barlucchi, L., Beltrami, A. P., Hintze, T. H., Nadal-Ginard, B., Kajstura, J., Leri, A., and Anversa, P.. 2001. "Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy." Circulation research 89 (3): 279-86. https://doi.org/10.1161/hh1501.094115
MLA 9 Cesselli, D., et al. "Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy." Circulation research, vol. 89, no. 3, 2001, pp. 279-86. doi:10.1161/hh1501.094115.
PMID 11485979 ↗
DOI 10.1161/hh1501.094115

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