The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Signaling Pathways in Reactive Oxygen Species–Induced Cardiomyocyte Apoptosis
Open accessAbstract
Background —The importance of free radical homeostasis and apoptosis in normal and diseased hearts and their interrelationships are poorly defined. We tested whether reactive oxygen species can trigger apoptosis in cardiomyocytes, and we explored the underlying pathways. Methods and Results —A cell culture model of isolated cardiac cells and different reactive oxygen species (ROS)–generating systems were used. Apoptosis became evident when cardiomyocytes were exposed to either H 2 O 2 or superoxide anion (O 2 − ). Both H 2 O 2 - and O 2 − -induced apoptosis of cardiomyocytes were associated with an increase in p53 protein content, whereas protein levels of Bax and Bcl-2 were unaltered. H 2 O 2 , but not O 2 − , induced an increase in the protein content of Bad. Furthermore, H 2 O 2 elicited translocation of Bax and Bad from cytosol to mitochondria, where these factors formed heterodimers with Bcl-2, which was followed by the release of cytochrome c , activation of CPP32, and cleavage of poly(ADP-ribose) polymerase. Interestingly, this pathway was not activated by O 2 − . Instead, O 2 − used Mch2α to promote the apoptotic pathway, as revealed by the activation of Mch2α and the cleavage of its substrate, lamin A. Conclusions —Taken together, these results indicate that ROS may play an important pathophysiological role in cardiac diseases characterized by apoptotic cell death and suggest that different ROS-induced activations of the apoptotic cell death program in cardiomyocytes involve distinct signaling pathways.
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Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c
Liu, X., Kim, C. N., Yang, J., Jemmerson, R., & Wang, X. (1996) · Cell · doi:10.1016/s0092-8674(00)80085-9 · Cited by 5,167
Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
Yang, J., Liu, X., Bhalla, K., Kim, C. N., Ibrado, A. M., Cai, J., Peng, T.-I., Jones, D. P., & Wang, X. (1997) · Science · doi:10.1126/science.275.5303.1129 · Cited by 4,911
The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
Kluck, R. M., Bossy-Wetzel, E., Green, D. R., & Newmeyer, D. D. (1997) · Science · doi:10.1126/science.275.5303.1132 · Cited by 4,714
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
A model for p53-induced apoptosis
Polyak, K., Xia, Y., Zweier, J. L., Kinzler, K. W., & Vogelstein, B. (1997) · Nature · doi:10.1038/38525 · Cited by 2,500
Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase
Li, Y., Huang, T.-T., Carlson, E. J., Melov, S., Ursell, P. C., Olson, J. L., Noble, L. J., Yoshimura, M. P., Berger, C., Chan, P. H., et al. (1995) · Nature Genetics · doi:10.1038/ng1295-376 · Cited by 1,789
Reperfusion injury induces apoptosis in rabbit cardiomyocytes.
Gottlieb, R. A., Burleson, K. O., Kloner, R. A., Babior, B. M., & Engler, R. L. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117504 · Cited by 1,441
Apoptosis in Myocytes in End-Stage Heart Failure
Narula, J., Haider, N., Virmani, R., DiSalvo, T. G., Kolodgie, F. D., Hajjar, R. J., Schmidt, U., Semigran, M. J., Dec, G. W., & Khaw, B.-A. (1996) · New England Journal of Medicine · doi:10.1056/nejm199610173351603 · Cited by 1,430
Direct measurement of free radical generation following reperfusion of ischemic myocardium.
Zweier, J. L., Flaherty, J. T., & Weisfeldt, M. L. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.5.1404 · Cited by 1,194
Kajstura, J., Cheng, W. N., Krzysztof Reiss, F., CLARK, W. A., Sonnenblick, E. H., Krajewski, S., Reed, J., Olivetti, G., & Anversa, P. (1996) · PubMed · Cited by 1,039
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Cellular Stress Responses: Cell Survival and Cell Death
Fulda, S., Gorman, A. M., Hori, O., & Samali, A. (2010) · International Journal of Cell Biology · doi:10.1155/2010/214074 · Cited by 1,519
Oxygen, oxidative stress, hypoxia, and heart failure
Giordano, F. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci200524408 · Cited by 1,496
Diabetic Cardiomyopathy: Evidence, Mechanisms, and Therapeutic Implications
Fang, Z. Y., Prins, J. B., & Marwick, T. H. (2004) · Endocrine Reviews · doi:10.1210/er.2003-0012 · Cited by 912
Myocardial Cell Death in Human Diabetes
Frustaci, A., Kajstura, J., Chimenti, C., Jakoniuk, I., Leri, A., Maseri, A., Nadal-Ginard, B., & Anversa, P. (2000) · Circulation Research · doi:10.1161/01.res.87.12.1123 · Cited by 796
Quagliaro, L., Piconi, L., Assaloni, R., Martinelli, L., Motz, E., & Ceriello, A. (2003) · Diabetes · doi:10.2337/diabetes.52.11.2795 · Cited by 769
Metadata
- Authors
- von Harsdorf, R., Li, P.-F., & Dietz, R.
- Venue
- Circulation
- Published
- 1999-06-08
- Volume
- 99
- Issue
- 22
- Pages
- 2934-2941
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1997832379
- Cited by
- 571
- References
- 26
- FWCI
- 10.00
- Type
- journal article
- Language
- en
- Open access
- bronze
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- von Harsdorf, R., Li, P.-F., & Dietz, R. (1999). Signaling Pathways in Reactive Oxygen Species–Induced Cardiomyocyte Apoptosis. Circulation. https://doi.org/10.1161/01.cir.99.22.2934
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