The DOI matches its Crossref record; 95 of the 95 references it cites were found in a registry or an index.
OPA1 processing in cell death and disease – the long and short of it
Abstract
The regulation of mitochondrial dynamics by the GTPase OPA1, which is located at the inner mitochondrial membrane, is crucial for adapting mitochondrial function and preserving cellular health. OPA1 governs the delicate balance between fusion and fission in the dynamic mitochondrial network. A disturbance of this balance, often observed under stress and pathologic conditions, causes mitochondrial fragmentation and can ultimately result in cell death. As discussed in this Commentary, these morphological changes are regulated by proteolytic processing of OPA1 by the inner-membrane peptidases YME1L (also known as YME1L1) and OMA1. Long, membrane-bound forms of OPA1 are required for mitochondrial fusion, but their processing to short, soluble forms limits fusion and can facilitate mitochondrial fission. Excessive OPA1 processing by the stress-activated protease OMA1 promotes mitochondrial fragmentation and, if persistent, triggers cell death and tissue degeneration in vivo. The prevention of OMA1-mediated OPA1 processing and mitochondrial fragmentation might thus offer exciting therapeutic potential for human diseases associated with mitochondrial dysfunction.
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Cites
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Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
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“Stimulated fission, combined with a reduced fusion capacity, can also help to isolate individual mitochondria from the network to facilitate their degradation by the selective autophagic process termed mitophagy (MacVicar and Lane, 2014; Twig et al., 2008).”
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OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
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Cited by
Mitochondrial dynamics: overview of molecular mechanisms
Tilokani, L., Nagashima, S., Paupe, V., & Prudent, J. (2018) · Essays in Biochemistry · doi:10.1042/ebc20170104 · Cited by 1,397
Quality control of the mitochondrion
Ng, M. Y. W., Wai, T., & Simonsen, A. (2021) · Developmental Cell · doi:10.1016/j.devcel.2021.02.009 · Cited by 445
Mitochondria, Bioenergetics and Apoptosis in Cancer
Burke, P. J. (2017) · Trends in Cancer · doi:10.1016/j.trecan.2017.10.006 · Cited by 432
Molecular basis of selective mitochondrial fusion by heterotypic action between OPA1 and cardiolipin
Ban, T., Ishihara, T., Kohno, H., Saita, S., Ichimura, A., Maenaka, K., Oka, T., Mihara, K., & Ishihara, N. (2017) · Nature Cell Biology · doi:10.1038/ncb3560 · Cited by 410
Cell biology of the mitochondrion
van der Bliek, A. M., Sedensky, M. M., & Morgan, P. G. (2017) · Genetics · doi:10.1534/genetics.117.300262 · Cited by 388
Metadata
- Authors
- MacVicar, T., & Langer, T.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2016-06-15
- Volume
- 129
- Issue
- 12
- Pages
- 2297-2306
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2399812166
- Cited by
- 426
- References
- 95
- FWCI
- 20.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Funders
- Deutsche Forschungsgemeinschaft
- European Research Council
- European Molecular Biology Organization
- Humboldt foundation
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