The DOI matches its Crossref record; 197 of the 197 references it cites were found in a registry or an index.
Ferroptosis and its potential role in the physiopathology of Parkinson’s Disease
Open accessAbstract
Parkinson's Disease (PD) is a common and progressive neurodegenerative disorder characterised by motor impairments as well as non-motor symptoms. While dopamine-based therapies are effective in fighting the symptoms in the early stages of the disease, a lack of neuroprotective drugs means that the disease continues to progress. Along with the traditionally recognised pathological hallmarks of dopaminergic neuronal death and intracellular α-synuclein (α-syn) depositions, iron accumulation, elevated oxidative stress and lipid peroxidation damage are further conspicuous features of PD pathophysiology. However, the underlying mechanisms linking these pathological hallmarks with neurodegeneration still remain unclear. Ferroptosis, a regulated iron dependent cell death pathway involving a lethal accumulation of lipid peroxides, shares several features with PD pathophysiology. Interestingly, α-syn has been functionally linked with the metabolism of both iron and lipid, suggesting a possible interplay between dysregulated α-syn and other PD pathological hallmarks related to ferroptosis. This review will address the importance for understanding these disease mechanisms that could be targeted therapeutically. Anti-ferroptosis molecules are neuroprotective in PD animal models and the anti-ferroptotic iron chelator, deferiprone, slowed disease progression and improved motor function in two independent clinical trials for PD. An ongoing larger multi-centre phase 2 clinical trial will confirm the therapeutic potential of deferiprone and the relevance of ferroptosis in PD. This review addresses the known pathological features of PD in relation to the ferroptosis pathway with therapeutic implications of targeting this cell death pathway.
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Oxidative Stress: Signaling Pathways, Biological Functions, and Disease
Liu, S., Liu, J., Wang, Y., Deng, F., & Deng, Z. (2025) · MedComm · doi:10.1002/mco2.70268 · Cited by 359
Phospholipase iPLA2β averts ferroptosis by eliminating a redox lipid death signal
Sun, W.-Y., Tyurin, V. A., Mikulska-Ruminska, K., Shrivastava, I. H., Anthonymuthu, T. S., Zhai, Y.-J., Pan, M.-H., Gong, H.-B., Lu, D.-H., Sun, J., et al. (2021) · Nature Chemical Biology · doi:10.1038/s41589-020-00734-x · Cited by 337
Yue, M., Wei, J., Chen, W., Hong, D., Chen, T., & Fang, X. (2022) · Nutrients · doi:10.3390/nu14224886 · Cited by 62
A review of proposed mechanisms for neurodegenerative disease
Kelser, B. M., Teichner, E. M., Subtirelu, R. C., & Hoss, K. N. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1370580 · Cited by 20
Metadata
- Authors
- Mahoney-Sánchez, L., Bouchaoui, H., Ayton, S., Devos, D., Duce, J. A., & Devedjian, J.-C.
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 196
- Pages
- 101890
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W3044551997
- Cited by
- 553
- References
- 197
- FWCI
- 22.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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