The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart
Open accessAbstract
Significance: Mitochondrial Ca 2+ is a fundamental signal that allows for adaptation to physiological stress but a liability during ischemia-reperfusion injury in heart. On one hand, mitochondrial Ca 2+ entry coordinates energy supply and demand in myocardium by increasing the activity of matrix dehydrogenases to augment ATP production by oxidative phosphorylation. On the other hand, inhibiting mitochondrial Ca 2+ overload is promulgated as a therapeutic approach to preserve myocardial tissue following ischemia-reperfusion injury. We developed a new mouse model of myocardial-targeted transgenic dominant-negative mitochondrial Ca 2+ uniporter (MCU) expression to test consequences of chronic loss of MCU-mediated Ca 2+ entry in heart. Here we show that MCU inhibition has unanticipated consequences on extramitochondrial pathways affecting oxygen utilization, cytoplasmic Ca 2+ homeostasis, physiologic responses to stress, and pathologic responses to ischemia-reperfusion injury.
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Baines, C. P., Kaiser, R. A., Purcell, N. H., Blair, N. S., Osinska, H., Hambleton, M. A., Brunskill, E. W., Sayen, M. R., Gottlieb, R. A., Dorn, G. W., et al. (2005) · Nature · doi:10.1038/nature03434 · Cited by 2,280 · cited 2×
“Excessive mitochondrial Ca entry promotes opening of the mitochondrial permeability transition pore, loss of ΔΨm (16), and release of mitochondrial reactive oxygen species (ROS) (17), which are consequences of ischemia-reperfusion injury that lead to myocardial death (18).”
BackgroundNakagawa, T., Shimizu, S., Watanabe, T., Yamaguchi, O., Otsu, K., Yamagata, H., Inohara, H., Kubo, T., & Tsujimoto, Y. (2005) · Nature · doi:10.1038/nature03317 · Cited by 1,635 · cited 1×
“Excessive mitochondrial Ca entry promotes opening of the mitochondrial permeability transition pore, loss of ΔΨm (16), and release of mitochondrial reactive oxygen species (ROS) (17), which are consequences of ischemia-reperfusion injury that lead to myocardial death (18).”
BackgroundRegulation of coronary blood flow during exercise
Duncker, D. J., & Bache, R. J. (2008) · Physiological Reviews · doi:10.1152/physrev.00045.2006 · Cited by 936
Superoxide flashes in single mitochondria
Wang, W., Fang, H., Groom, L., Cheng, A., Zhang, W., Liu, J., Wang, X., Li, K., Han, P., Zheng, M., et al. (2008) · Cell · doi:10.1016/j.cell.2008.06.017 · Cited by 715
Mitochondrial Energetics in the Heart in Obesity-Related Diabetes
Boudina, S., Sena, S., Theobald, H., Sheng, X., Wright, J. J., Hu, X. X., Aziz, S., Johnson, J. I., Bugger, H., Zaha, V. G., et al. (2007) · Diabetes · doi:10.2337/db07-0481 · Cited by 586
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Cited by
The machineries, regulation and cellular functions of mitochondrial calcium
Giorgi, C., Marchi, S., & Pinton, P. (2018) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0052-8 · Cited by 941
Enjoy the Trip: Calcium in Mitochondria Back and Forth
De Stefani, D., Rizzuto, R., & Pozzan, T. (2016) · Annual Review of Biochemistry · doi:10.1146/annurev-biochem-060614-034216 · Cited by 423
Mitochondrial calcium exchange in physiology and disease
Garbincius, J. F., & Elrod, J. W. (2022) · Physiological Reviews · doi:10.1152/physrev.00041.2020 · Cited by 412
Mitochondrial Function and Dysfunction in Dilated Cardiomyopathy
Ramaccini, D., Montoya-Uribe, V., Aan, F. J., Modesti, L., Potes, Y., Wieckowski, M. R., Krga, I., Glibetić, M., Pinton, P., Giorgi, C., et al. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.624216 · Cited by 136
Bround, M. J., Abay, E., Huo, J., Havens, J. R., York, A. J., Bers, D. M., & Molkentin, J. D. (2024) · Scientific Reports · doi:10.1038/s41598-024-57340-3 · Cited by 20
Metadata
- Authors
- Rasmussen, T. P., Wu, Y., Joiner, M.-L. A., Koval, O. M., Wilson, N. R., Luczak, E. D., Wang, Q., Chen, B., Gao, Z., Zhu, Z., Wagner, B. A., Soto, J., McCormick, M. L., Kutschke, W., Weiss, R. M., Yu, L., Boudreau, R. L., Abel, E. D., Zhan, F., Spitz, D. R., Buettner, G. R., Song, L.-S., Zingman, L. V., & Anderson, M. E.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2015-07-07
- Volume
- 112
- Issue
- 29
- Pages
- 9129-9134
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1547216871
- Cited by
- 162
- References
- 5
- FWCI
- 6.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Rasmussen, T. P., Wu, Y., Joiner, M.-L. A., Koval, O. M., Wilson, N. R., Luczak, E. D., Wang, Q., Chen, B., Gao, Z., Zhu, Z., Wagner, B. A., Soto, J., McCormick, M. L., Kutschke, W., Weiss, R. M., Yu, L., Boudreau, R. L., Abel, E. D., Zhan, F., . . . Anderson, M. E. (2015). Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1504705112
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