The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.
PINK1/PARKIN signalling in neurodegeneration and neuroinflammation
Open accessAbstract
Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson’s disease (PD). PINK1, a protein kinase, and PARKIN, an E3 ubiquitin ligase, control the specific elimination of dysfunctional or superfluous mitochondria, thus fine-tuning mitochondrial network and preserving energy metabolism. PINK1 regulates PARKIN translocation in impaired mitochondria and drives their removal via selective autophagy, a process known as mitophagy. As knowledge obtained using different PINK1 and PARKIN transgenic animal models is being gathered, growing evidence supports the contribution of mitophagy impairment to several human pathologies, including PD and Alzheimer’s diseases (AD). Therefore, therapeutic interventions aiming to modulate PINK1/PARKIN signalling might have the potential to treat these diseases. In this review, we will start by discussing how the interplay of PINK1 and PARKIN signalling helps mediate mitochondrial physiology. We will continue by debating the role of mitochondrial dysfunction in disorders such as amyotrophic lateral sclerosis, Alzheimer’s, Huntington’s and Parkinson’s diseases, as well as eye diseases such as age-related macular degeneration and glaucoma, and the causative factors leading to PINK1/PARKIN-mediated neurodegeneration and neuroinflammation. Finally, we will discuss PINK1/PARKIN gene augmentation possibilities with a particular focus on AD, PD and glaucoma.
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Cites
1 retracted
RETRACTED ARTICLE: Parkin and PINK1 mitigate STING-induced inflammation
Sliter, D. A., Martinez, J., Hao, L., Chen, X., Sun, N., Fischer, T. D., Burman, J. L., Li, Y., Zhang, Z., Narendra, D. P., et al. (2018) · Nature · doi:10.1038/s41586-018-0448-9 · Cited by 1,287
RetractedMutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
Structural absorption by barbule microstructures of super black bird of paradise feathers
McCoy, D. E., Feo, T., Harvey, T. A., & Prum, R. O. (2018) · Nature Communications · doi:10.1038/s41467-017-02088-w · Cited by 7,424
Global Prevalence of Glaucoma and Projections of Glaucoma Burden through 2040
Tham, Y.-C., Li, X., Wong, T. Y., Quigley, H. A., Aung, T., & Cheng, C.-Y. (2014) · Ophthalmology · doi:10.1016/j.ophtha.2014.05.013 · Cited by 7,159
Rosen, D. R., Siddique, T., Patterson, D., Figlewicz, D. A., Sapp, P., Hentati, A., Donaldson, D., Goto, J., O'Regan, J. P., Deng, H.-X., et al. (1993) · Nature · doi:10.1038/362059a0 · Cited by 7,062
Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis
Neumann, M., Sampathu, D. M., Kwong, L. K., Truax, A. C., Micsenyi, M. C., Chou, T. T., Bruce, J., Schuck, T., Grossman, M., Clark, C. M., et al. (2006) · Science · doi:10.1126/science.1134108 · Cited by 6,576
Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
Kitada, T., Asakawa, S., Hattori, N., Matsumine, H., Yamamura, Y., Minoshima, S., Yokochi, M., Mizuno, Y., & Shimizu, N. (1998) · Nature · doi:10.1038/33416 · Cited by 5,227
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Mitochondrial Fission, Fusion, and Stress
Youle, R. J., & van der Bliek, A. M. (2012) · Science · doi:10.1126/science.1219855 · Cited by 3,674 · cited 2×
“If left unchecked, these processes can cause damage to nucleic acids, lipids and proteins through ROS, resulting in sustained oxidative stress [16, 17].”
BackgroundHereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
Cited by
Lee, J., & Kim, H.-J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.931536 · Cited by 310
Oxidative stress and mitochondrial impairment: Key drivers in neurodegenerative disorders
Wen, P., Sun, Z., Gou, F., Wang, J., Fan, Q., Zhao, D., & Yang, L. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102667 · Cited by 253
Mitophagy and cGAS–STING crosstalk in neuroinflammation
Zhou, X., Wang, J., Yu, L., Qiao, G., Qin, D., Yuen-Kwan Law, B., Ren, F., Wu, J., & Wu, A. (2024) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2024.05.012 · Cited by 131
TRAP1 in Oxidative Stress and Neurodegeneration
Ramos Rego, I., Santos Cruz, B., Ambrósio, A. F., & Alves, C. H. (2021) · Antioxidants · doi:10.3390/antiox10111829 · Cited by 44
Self-citationE3 ubiquitin ligases and their therapeutic potential in disease Management
Madhukar, G., Haque, M. A., Khan, S., Kim, J.-J., & Danishuddin (2025) · Biochemical Pharmacology · doi:10.1016/j.bcp.2025.116875 · Cited by 26
Metadata
- Authors
- Quinn, P. M. J., Moreira, P. I., Ambrósio, A. F., & Alves, C. H.
- Venue
- Acta Neuropathologica Communications
- Published
- 2020-11-09
- Volume
- 8
- Issue
- 1
- Pages
- 189-189
- ISSN
- 2051-5960 (ISSN-L)
- OpenAlex
- W3103775593
- Cited by
- 481
- References
- 225
- FWCI
- 18.46
- Type
- journal article
- Language
- en
- Open access
- gold
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- Quinn, P. M. J., Moreira, P. I., Ambrósio, A. F., & Alves, C. H. (2020). PINK1/PARKIN signalling in neurodegeneration and neuroinflammation. Acta Neuropathologica Communications. https://doi.org/10.1186/s40478-020-01062-w
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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.
