The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Mitochondrial OPA1, apoptosis, and heart failure
Open accessAbstract
AIMS: Mitochondrial fusion and fission are essential processes for preservation of normal mitochondrial function. We hypothesized that fusion proteins would be decreased in heart failure (HF), as the mitochondria in HF have been reported to be small and dysfunctional. METHODS AND RESULTS: Expression of optic atrophy 1 (OPA1), a mitochondrial fusion protein, was decreased in both human and rat HF, as observed by western blotting. OPA1 is important for maintaining normal cristae structure and function, for preserving the inner membrane structure and for protecting cells from apoptosis. Confocal and electron microscopy studies demonstrated that the mitochondria in the failing hearts were small and fragmented, consistent with decreased fusion. OPA1 mRNA levels did not differ between failing and normal hearts, suggesting post-transcriptional control. Simulated ischaemia in the cardiac myogenic cell line H9c2 cells reduced OPA protein levels. Reduction of OPA1 expression with shRNA resulted in increased apoptosis and fragmentation of the mitochondria. Overexpression of OPA1 increased mitochondrial tubularity, but did not protect against simulated ischaemia-induced apoptosis. Cytochrome c release from the mitochondria was increased both with reduction in OPA1 and with overexpression of OPA1. CONCLUSION: This is the first report, to our knowledge, of changes in mitochondrial fusion/fission proteins in cardiovascular disease. These changes have implications for mitochondrial function and apoptosis, contributing to the cell loss which is part of the downward progression of the failing heart.
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Cites
OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Frezza, C., Cipolat, S., Martins de Brito, O., Micaroni, M., Beznoussenko, G. V., Rudka, T., Bartoli, D., Polishuck, R. S., Danial, N. N., De Strooper, B., et al. (2006) · Cell · doi:10.1016/j.cell.2006.06.025 · Cited by 1,673
Apoptosis in the Failing Human Heart
Olivetti, G., Abbi, R., Quaini, F., Kajstura, J., Cheng, W., Nitahara, J. A., Quaini, E., Di Loreto, C., Beltrami, C. A., Krajewski, S., et al. (1997) · New England Journal of Medicine · doi:10.1056/nejm199704173361603 · Cited by 1,673
Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376 · cited 11×
“In the current study, OPA1 was decreased in the mitochondria in ischaemic HF, and based on the studies in the Drosophila and MEF cells, this might be expected to impair function, consistent with the decrease in ATP levels seen in HF.12,29 To better understand the function of OPA1, further studies are needed on the eff…”
BackgroundResultInfluentialCassidy-Stone, A., Chipuk, J. E., Ingerman, E., Song, C., Yoo, C., Kuwana, T., Kurth, M. J., Shaw, J. T., Hinshaw, J. E., Green, D. R., et al. (2008) · Developmental Cell · doi:10.1016/j.devcel.2007.11.019 · Cited by 1,200
Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosis
Lee, Y.-J., Jeong, S.-Y., Karbowski, M., Smith, C. L., & Youle, R. J. (2004) · Molecular Biology of the Cell · doi:10.1091/mbc.e04-04-0294 · Cited by 1,042
OPA1 mutations induce mitochondrial DNA instability and optic atrophy 'plus' phenotypes
Amati-Bonneau, P., Valentino, M. L., Reynier, P., Gallardo, M. E., Bornstein, B., Boissiere, A., Campos, Y., Rivera, H., de la Aleja, J. G., Carroccia, R., et al. (2008) · Brain · doi:10.1093/brain/awm298 · Cited by 520
Cardiac mitochondrial damage and biogenesis in a chronic model of type 1 diabetes
Shen, X., Zheng, S., Thongboonkerd, V., Xu, M., Pierce, W. M., Klein, J. B., & Epstein, P. N. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00047.2004 · Cited by 258
Molecular Mechanisms in Heart Failure
Hilfiker-Kleiner, D., Landmesser, U., & Drexler, H. (2006) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2006.07.007 · Cited by 151
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Mitochondrial dynamics, mitophagy and cardiovascular disease
Vásquez‐Trincado, C., García‐Carvajal, I., Pennanen, C., Parra, V., Hill, J. A., Rothermel, B. A., & Lavandero, S. (2016) · The Journal of Physiology · doi:10.1113/jp271301 · Cited by 629
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Merz, K. E., & Thurmond, D. C. (2020) · Comprehensive Physiology · doi:10.1002/cphy.c190029 · Cited by 494
Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases
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SIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress
Samant, S. A., Zhang, H. J., Hong, Z., Pillai, V. B., Sundaresan, N. R., Wolfgeher, D., Archer, S. L., Chan, D. C., & Gupta, M. P. (2014) · Molecular and Cellular Biology · doi:10.1128/mcb.01483-13 · Cited by 446
Metadata
- Authors
- Chen, L., Gong, Q., Stice, J. P., & Knowlton, A. A.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-06-03
- Volume
- 84
- Issue
- 1
- Pages
- 91-99
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- OpenAlex
- W2108482197
- Cited by
- 426
- References
- 8
- FWCI
- 6.84
- Type
- journal article
- Language
- en
- Open access
- bronze
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