The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Mitofusin-2 Maintains Mitochondrial Structure and Contributes to Stress-Induced Permeability Transition in Cardiac Myocytes
Open accessAbstract
Mitofusin-2 (Mfn-2) is a dynamin-like protein that is involved in the rearrangement of the outer mitochondrial membrane. Research using various experimental systems has shown that Mfn-2 is a mediator of mitochondrial fusion, an evolutionarily conserved process responsible for the surveillance of mitochondrial homeostasis. Here, we find that cardiac myocyte mitochondria lacking Mfn-2 are pleiomorphic and have the propensity to become enlarged. Consistent with an underlying mild mitochondrial dysfunction, Mfn-2-deficient mice display modest cardiac hypertrophy accompanied by slight functional deterioration. The absence of Mfn-2 is associated with a marked delay in mitochondrial permeability transition downstream of Ca(2+) stimulation or due to local generation of reactive oxygen species (ROS). Consequently, Mfn-2-deficient adult cardiomyocytes are protected from a number of cell death-inducing stimuli and Mfn-2 knockout hearts display better recovery following reperfusion injury. We conclude that in cardiac myocytes, Mfn-2 controls mitochondrial morphogenesis and serves to predispose cells to mitochondrial permeability transition and to trigger cell death.
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Citations
Cites
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
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Mitochondria and cell death: outer membrane permeabilization and beyond
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Mitofusin 2 tethers endoplasmic reticulum to mitochondria
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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
Close Contacts with the Endoplasmic Reticulum as Determinants of Mitochondrial Ca 2+ Responses
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OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
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“Finally, Mfn-2-null hearts display significant protection from ischemia/reperfusion injury an effect also observed in Cyp-Dnull hearts (8, 60).”
BackgroundMutations in the mitochondrial GTPase mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A
Züchner, S., Mersiyanova, I. V., Muglia, M., Bissar-Tadmouri, N., Rochelle, J., Dadali, E. L., Zappia, M., Nelis, E., Patitucci, A., Senderek, J., et al. (2004) · Nature Genetics · doi:10.1038/ng1341 · Cited by 1,572
Reactive Oxygen Species (Ros-Induced) Ros Release
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Cited by
PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress
Verfaillie, T., Rubio, N., Garg, A. D., Bultynck, G., Rizzuto, R., Decuypere, J.-P., Piette, J., Linehan, C., Gupta, S., Samali, A., et al. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2012.74 · Cited by 850
Sebastián, D., Hernández-Alvarez, M. I., Segalés, J., Sorianello, E., Muñoz, J. P., Sala, D., Waget, A., Liesa, M., Paz, J. C., Gopalacharyulu, P., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1108220109 · Cited by 673
The Role of Autophagy in the Heart
Sciarretta, S., Maejima, Y., Zablocki, D., & Sadoshima, J. (2018) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021317-121427 · Cited by 547
Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice
Wai, T., García-Prieto, J., Baker, M. J., Merkwirth, C., Benit, P., Rustin, P., Rupérez, F. J., Barbas, C., Ibañez, B., & Langer, T. (2015) · Science · doi:10.1126/science.aad0116 · Cited by 551
Mitofusin 2 in POMC neurons connects ER stress with leptin resistance and energy imbalance
Schneeberger, M., Dietrich, M. O., Sebastián, D., Imbernón, M., Castaño, C., Garcia, A., Esteban, Y., Gonzalez-Franquesa, A., Rodríguez, I. C., Bortolozzi, A., et al. (2013) · Cell · doi:10.1016/j.cell.2013.09.003 · Cited by 519
Metadata
- Authors
- Papanicolaou, K. N., Khairallah, R. J., Ngoh, G. A., Chikando, A., Luptak, I., O'Shea, K. M., Riley, D. D., Lugus, J. J., Colucci, W. S., Lederer, W. J., Stanley, W. C., & Walsh, K.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2011-03-01
- Volume
- 31
- Issue
- 6
- Pages
- 1309-1328
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2107030671
- Cited by
- 358
- References
- 28
- FWCI
- 10.82
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Mitofusin-2 Maintains Mitochondrial Structure and Contributes to Stress-Induced Permeability Transition in Cardiac Myocytes. https://app.cochat.ai/papers/10.1128/mcb.00911-10
- The paper
- Papanicolaou, K. N., Khairallah, R. J., Ngoh, G. A., Chikando, A., Luptak, I., O'Shea, K. M., Riley, D. D., Lugus, J. J., Colucci, W. S., Lederer, W. J., Stanley, W. C., & Walsh, K. (2011). Mitofusin-2 Maintains Mitochondrial Structure and Contributes to Stress-Induced Permeability Transition in Cardiac Myocytes. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.00911-10
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
