The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Knockout mice heterozygous for Sod2 show alterations in cardiac mitochondrial function and apoptosis
Abstract
Heart mitochondria from heterozygous ( Sod2−/+) knockout mice have a 50% reduction in manganese superoxide dismutase (MnSOD) activity. The decrease in MnSOD activity was associated with increased mitochondrial oxidative damage as demonstrated by a decrease in the activities of iron sulfhydryl proteins sensitive to oxygen stress (aconitase and reduced nicotinamide adenine dinucleotide-oxidoreductase). Mitochondrial function was altered in the Sod2−/+mice, as shown by decreased respiration by complex I and an increase in the sensitivity of the permeability transition to induction by calcium and t-butylhydroperoxide. The increased induction of the permeability transition in heart mitochondria from Sod2−/+.mice was associated with increased release of cytochrome c and an increase in DNA fragmentation. Cardiomyocytes isolated from neonatal Sod2−/+and Sod2−/−mice were more sensitive to cell death than cardiomyocytes from Sod2+/+mice after t-butylhydroperoxide treatment, and this increased sensitivity was prevented by inhibiting the permeability transition with cyclosporin A. These experiments demonstrate that MnSOD may play an important role in the induction of the mitochondrial pathway of apoptosis in the heart, and this appears to occur primarily through the permeability transition.
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Cites
Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase
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Self-citationBax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of Apoptosis
Marzo, I., Brenner, C., Zamzami, N., Jürgensmeier, J. M., Susin, S. A., Vieira, H. L. A., Prévost, M.-C., Xie, Z., Matsuyama, S., Reed, J. C., et al. (1998) · Science · doi:10.1126/science.281.5385.2027 · Cited by 1,168
Keller, J. N., Kindy, M. S., Holtsberg, F. W., St. Clair, D. K., Yen, H.-C., Germeyer, A., Steiner, S. M., Bruce-Keller, A. J., Hutchins, J. B., & Mattson, M. P. (1998) · The Journal of Neuroscience · doi:10.1523/jneurosci.18-02-00687.1998 · Cited by 863
Broekemeier, K. M., Dempsey, M. E., & Pfeiffer, D. R. (1989) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)83116-7 · Cited by 699
Costantini, P., Belzacq, A.-S., Vieira, H. L., Larochette, N., de Pablo, M. A., Zamzami, N., Susin, S. A., Brenner, C., & Kroemer, G. (2000) · Oncogene · doi:10.1038/sj.onc.1203299 · Cited by 284
Superoxides from mitochondrial complex III: the role of manganese superoxide dismutase
Raha, S., McEachern, G. E., Myint, A. T., & Robinson, B. H. (2000) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(00)00338-5 · Cited by 223
Cited by
Mitochondrial metabolism of reactive oxygen species
Andreyev, A. Y., Kushnareva, Y. E., & Starkov, A. A. (2005) · Biochemistry (Moscow) · doi:10.1007/s10541-005-0102-7 · Cited by 1,336
Trends in oxidative aging theories
Muller, F. L., Lustgarten, M. S., Jang, Y., Richardson, A., & Van Remmen, H. (2007) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2007.03.034 · Cited by 1,053
Self-citationMitochondrial dysfunction and oxidative stress in heart disease
Peoples, J. N., Saraf, A., Ghazal, N., Pham, T. T., & Kwong, J. Q. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0355-7 · Cited by 950
Van Remmen, H., Ikeno, Y., Hamilton, M., Pahlavani, M., Wolf, N., Thorpe, S. R., Alderson, N. L., Baynes, J. W., Epstein, C. J., Huang, T.-T., et al. (2003) · Physiological Genomics · doi:10.1152/physiolgenomics.00122.2003 · Cited by 734
Self-citationSuperoxide Dismutases in the Lung and Human Lung Diseases
Kinnula, V. L., & Crapo, J. D. (2003) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200212-1479so · Cited by 620
Metadata
- Authors
- Van Remmen, H., Williams, M. D., Guo, Z., Estlack, L., Yang, H., Carlson, E. J., Epstein, C. J., Huang, T. T., & Richardson, A.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2001-09-01
- Volume
- 281
- Issue
- 3
- Pages
- H1422-H1432
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W45625719
- Cited by
- 230
- References
- 6
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Knockout mice heterozygous for Sod2 show alterations in cardiac mitochondrial function and apoptosis. https://app.cochat.ai/papers/10.1152/ajpheart.2001.281.3.h1422
- The paper
- Van Remmen, H., Williams, M. D., Guo, Z., Estlack, L., Yang, H., Carlson, E. J., Epstein, C. J., Huang, T. T., & Richardson, A. (2001). Knockout mice heterozygous for Sod2 show alterations in cardiac mitochondrial function and apoptosis. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.2001.281.3.h1422
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