The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
Mitochondrial morphology and cardiovascular disease
Open accessAbstract
Mitochondria are dynamic and are able to interchange their morphology between elongated interconnected mitochondrial networks and a fragmented disconnected arrangement by the processes of mitochondrial fusion and fission, respectively. Changes in mitochondrial morphology are regulated by the mitochondrial fusion proteins (mitofusins 1 and 2, and optic atrophy 1) and the mitochondrial fission proteins (dynamin-related peptide 1 and mitochondrial fission protein 1) and have been implicated in a variety of biological processes including embryonic development, metabolism, apoptosis, and autophagy, although the majority of studies have been largely confined to non-cardiac cells. Despite the unique arrangement of mitochondria in the adult heart, emerging data suggest that changes in mitochondrial morphology may be relevant to various aspects of cardiovascular biology-these include cardiac development, the response to ischaemia-reperfusion injury, heart failure, diabetes mellitus, and apoptosis. Interestingly, the machinery required for altering mitochondrial shape in terms of the mitochondrial fusion and fission proteins are all present in the adult heart, but their physiological function remains unclear. In this article, we review the current developments in this exciting new field of mitochondrial biology, the implications for cardiovascular physiology, and the potential for discovering novel therapeutic strategies for treating cardiovascular disease.
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Citations
Cites
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Twig, G., Elorza, A., Molina, A. J. A., Mohamed, H., Wikstrom, J. D., Walzer, G., Stiles, L., Haigh, S. E., Katz, S., Las, G., et al. (2008) · The EMBO Journal · doi:10.1038/sj.emboj.7601963 · Cited by 3,082 · cited 6×
“Furthermore, blocking OPA1 with siRNA induced mitochondrial fragmentation and apoptotic cell death, although the over-expression of OPA-1 did not protect the cells against ischaemia-induced apoptosis.89 Of note, the pre-treatment of cells with cyclosporin A (CsA), a known mPTP inhibitor,90 prevented the reduction in O…”
BackgroundInfluentialChen, H., Detmer, S. A., Ewald, A. J., Griffin, E. E., Fraser, S. E., & Chan, D. C. (2003) · The Journal of Cell Biology · doi:10.1083/jcb.200211046 · Cited by 2,601
Mitofusin 2 tethers endoplasmic reticulum to mitochondria
de Brito, O. M., & Scorrano, L. (2008) · Nature · doi:10.1038/nature07534 · Cited by 2,442
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
Mutations 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
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 3×
“However, the over-expression of OPA1 did not improve mitochondrial respiration.(64) Interestingly, knock-down of the mitochondrial fission protein, Drp1, has similar effects on mitochondrial metabolism,(66) suggesting that any alteration in the mitochondrial network appears to impact on metabolism in a negative way.”
BackgroundYu, T., Robotham, J. L., & Yoon, Y. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0511154103 · Cited by 1,246
Mitotic phosphorylation of dynamin-related GTPase Drp1 participates in mitochondrial fission.
Taguchi, N., Ishihara, N., Jofuku, A., Oka, T., & Mihara, K. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m607279200 · Cited by 1,226
Cassidy-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
Cited by
Energy metabolism in health and diseases
Liu, H., Wang, S., Wang, J., Guo, X., Song, Y., Fu, K., Gao, Z., Liu, D., He, W., & Yang, L.-L. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02141-x · Cited by 399
Disatnik, M., Ferreira, J. C. B., Campos, J. C., Gomes, K. S., Dourado, P. M. M., Qi, X., & Mochly‐Rosen, D. (2013) · Journal of the American Heart Association · doi:10.1161/jaha.113.000461 · Cited by 334
Ong, S.-B., Samangouei, P., Kalkhoran, S. B., & Hausenloy, D. J. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2014.11.005 · Cited by 323
Self-citationImpaired Mitochondrial Dynamics and Bioenergetics in Diabetic Skeletal Muscle
Liu, R., Jin, P., LiqunYu, Wang, Y., Han, L., Shi, T., & Li, X. (2014) · PLoS ONE · doi:10.1371/journal.pone.0092810 · Cited by 146
Pride, C. K., Mo, L., Quesnelle, K., Dagda, R. K., Murillo, D., Geary, L., Corey, C., Portella, R., Zharikov, S., St Croix, C., et al. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvt224 · Cited by 97
Metadata
- Authors
- Ong, S.-B., & Hausenloy, D. J.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-07-14
- Volume
- 88
- Issue
- 1
- Pages
- 16-29
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2120379299
- Cited by
- 323
- References
- 25
- FWCI
- 6.85
- Type
- journal article
- Language
- en
- Open access
- green
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