The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Axonal Degeneration Is Mediated by the Mitochondrial Permeability Transition Pore
Open accessAbstract
Axonal degeneration is an active process that has been associated with neurodegenerative conditions triggered by mechanical, metabolic, infectious, toxic, hereditary and inflammatory stimuli. This degenerative process can cause permanent loss of function, so it represents a focus for neuroprotective strategies. Several signaling pathways are implicated in axonal degeneration, but identification of an integrative mechanism for this self-destructive process has remained elusive. Here, we show that rapid axonal degeneration triggered by distinct mechanical and toxic insults is dependent on the activation of the mitochondrial permeability transition pore (mPTP). Both pharmacological and genetic targeting of cyclophilin D, a functional component of the mPTP, protects severed axons and vincristine-treated neurons from axonal degeneration in ex vivo and in vitro mouse and rat model systems. These effects were observed in axons from both the peripheral and central nervous system. Our results suggest that the mPTP is a key effector of axonal degeneration, upon which several independent signaling pathways converge. Since axonal and synapse degeneration are increasingly considered early pathological events in neurodegeneration, our work identifies a potential target for therapeutic intervention in a wide variety of conditions that lead to loss of axons and subsequent functional impairment.
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Cites
Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes
Liu, J., Farmer, J. D., Lane, W. S., Friedman, J., Weissman, I., & Schreiber, S. L. (1991) · Cell · doi:10.1016/0092-8674(91)90124-h · Cited by 4,116 · cited 1×
“CsA can inhibit the mPTP through its interaction with CypD, but it also has immunosuppressant actions through calcineurin inhibition (Liu et al., 1991).”
BackgroundBaines, 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
Nakagawa, 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×
“Genetic ablation studies have only confirmed a role for CypD in mPTP-mediated cell death (Baines et al., 2005; Nakagawa et al., 2005; Schinzel et al., 2005).”
BackgroundIncreased Nuclear NAD Biosynthesis and SIRT1 Activation Prevent Axonal Degeneration
Araki, T., Sasaki, Y., & Milbrandt, J. (2004) · Science · doi:10.1126/science.1098014 · Cited by 1,060
Axon degeneration mechanisms: Commonality amid diversity
Coleman, M. (2005) · Nature reviews. Neuroscience · doi:10.1038/nrn1788 · Cited by 819
Absence of Wallerian Degeneration does not Hinder Regeneration in Peripheral Nerve
Lunn, E. R., Perry, V. H., Brown, M. C., Rosen, H., & Gordon, S. (1989) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.1989.tb00771.x · Cited by 646
Kuchibhotla, K. V., Goldman, S. T., Lattarulo, C. R., Wu, H.-Y., Hyman, B. T., & Bacskai, B. J. (2008) · Neuron · doi:10.1016/j.neuron.2008.06.008 · Cited by 614
Hetz, C., Thielen, P., Matus, S., Nassif, M., Court, F., Kiffin, R., Martinez, G., Cuervo, A. M., Brown, R. H., & Glimcher, L. H. (2009) · Genes & Development · doi:10.1101/gad.1830709 · Cited by 530 · cited 1×
“Mouse embryonic fibroblast (MEF) cells with reduced levels of CypD were generated by using methods previously described (Hetz et al., 2009).”
MethodSelf-citationBerger, F., Lau, C., Dahlmann, M., & Ziegler, M. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m508660200 · Cited by 508
Endogenous Nmnat2 Is an Essential Survival Factor for Maintenance of Healthy Axons
Gilley, J., & Coleman, M. P. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000300 · Cited by 472
Cited by
Axon degeneration in Parkinson's disease
Burke, R. E., & O'Malley, K. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2012.01.011 · Cited by 493
Schwann cell‐derived exosomes enhance axonal regeneration in the peripheral nervous system
Lopez‐Verrilli, M. A., Picou, F., & Court, F. A. (2013) · Glia · doi:10.1002/glia.22558 · Cited by 453
Self-citationLipid peroxidation and neurodegenerative disease
Reed, T. T. (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.06.027 · Cited by 379
Castillo, K., Nassif, M., Valenzuela, V., Rojas, F., Matus, S., Mercado, G., Court, F. A., van Zundert, B., & Hetz, C. (2013) · Autophagy · doi:10.4161/auto.25188 · Cited by 340
Self-citationAxon Self-Destruction: New Links among SARM1, MAPKs, and NAD+ Metabolism
Gerdts, J., Summers, D. W., Milbrandt, J., & DiAntonio, A. (2016) · Neuron · doi:10.1016/j.neuron.2015.12.023 · Cited by 320
Metadata
- Authors
- Barrientos, S. A., Martinez, N. W., Yoo, S., Jara, J. S., Zamorano, S., Hetz, C., Twiss, J. L., Alvarez, J., & Court, F. A.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-01-19
- Volume
- 31
- Issue
- 3
- Pages
- 966-978
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2003682409
- Cited by
- 207
- References
- 15
- FWCI
- 8.82
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- The paper
- Barrientos, S. A., Martinez, N. W., Yoo, S., Jara, J. S., Zamorano, S., Hetz, C., Twiss, J. L., Alvarez, J., & Court, F. A. (2011). Axonal Degeneration Is Mediated by the Mitochondrial Permeability Transition Pore. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.4065-10.2011
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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