The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Two molecular pathways initiate mitochondria-dependent dopaminergic neurodegeneration in experimental Parkinson's disease
Open accessAbstract
Dysfunction of mitochondrial complex I is associated with a wide spectrum of neurodegenerative disorders, including Parkinson's disease (PD). In rodents, inhibition of complex I leads to degeneration of dopaminergic neurons of the substantia nigra pars compacta (SNpc), as seen in PD, through activation of mitochondria-dependent apoptotic molecular pathways. In this scenario, complex I blockade increases the soluble pool of cytochrome c in the mitochondrial intermembrane space through oxidative mechanisms, whereas activation of pro-cell death protein Bax is actually necessary to trigger neuronal death by permeabilizing the outer mitochondrial membrane and releasing cytochrome c into the cytosol. Activation of Bax after complex I inhibition relies on its transcriptional induction and translocation to the mitochondria. How complex I deficiency leads to Bax activation is currently unknown. Using gene-targeted mice, we show that the tumor suppressor p53 mediates Bax transcriptional induction after PD-related complex I blockade in vivo , but it does not participate in Bax mitochondrial translocation in this model, either by a transcription-independent mechanism or through the induction of BH3-only proteins Puma or Noxa. Instead, Bax mitochondrial translocation in this model relies mainly on the JNK-dependent activation of the BH3-only protein Bim. Targeting either Bax transcriptional induction or Bax mitochondrial translocation results in a marked attenuation of SNpc dopaminergic cell death caused by complex I inhibition. These results provide further insight into the pathogenesis of PD neurodegeneration and identify molecular targets of potential therapeutic significance for this disabling neurological illness.
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Cites
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Cited by
Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins
Singh, R., Letai, A., & Sarosiek, K. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0089-8 · Cited by 2,111
Pathogenic Lysosomal Depletion in Parkinson's Disease
Dehay, B., Bové, J., Rodríguez-Muela, N., Perier, C., Recasens, A., Boya, P., & Vila, M. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.1920-10.2010 · Cited by 825
Self-citationMissing pieces in the Parkinson's disease puzzle
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Mitochondrial dysfunction in Parkinson's disease
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PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons
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Metadata
- Authors
- Perier, C., Bové, J., Wu, D.-C., Dehay, B., Choi, D.-K., Jackson-Lewis, V., Rathke-Hartlieb, S., Bouillet, P., Strasser, A., Schulz, J. B., Przedborski, S., & Vila, M.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2007-05-08
- Volume
- 104
- Issue
- 19
- Pages
- 8161-8166
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2060457554
- Cited by
- 229
- References
- 13
- FWCI
- 12.90
- Type
- journal article
- Language
- en
- Open access
- green
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- Perier, C., Bové, J., Wu, D.-C., Dehay, B., Choi, D.-K., Jackson-Lewis, V., Rathke-Hartlieb, S., Bouillet, P., Strasser, A., Schulz, J. B., Przedborski, S., & Vila, M. (2007). Two molecular pathways initiate mitochondria-dependent dopaminergic neurodegeneration in experimental Parkinson's disease. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0609874104
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Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
