The DOI matches its Crossref record; 114 of the 115 references it cites were found in a registry or an index.
Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.
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In the citing paper
“mitochondrial malfunction is increasingly considered a key determinant of dopaminergic neurodegeneration, serving as an overlapping risk factor for both sporadic and familial cases [11]”
From Healthy Human Fecal Microbiota Transplantation into Mice Attenuates MPTP-Induced Neurotoxicity via AMPK/SOD2 Pathway (2023) · cites this paper as [11]
In the citing paper
“it has been associated with a number of age-related diseases such as neurological disorders, CVD, liver and kidney diseases, diabetes and cancer”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Ryan et al., 2015
In the citing paper
“it has been associated with a number of age-related diseases such as neurological disorders, cardiovascularCVD, liver and kidney diseases, diabetes and cancer (Lane et al., 2015; Payne and Chinnery, 2015; Ryan et al., 2015; Wallace, 2012).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Ryan et al., 2015
Citations
Cites
1 retracted
TOM40 Mediates Mitochondrial Dysfunction Induced by α-Synuclein Accumulation in Parkinson’s Disease
Bender, A., Desplats, P., Spencer, B. J., Rockenstein, E. M., Adame, A., Elstner, M., Laub, C., Mueller, S. K., Koob, A. O., Mante, M., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0062277 · Cited by 151
RetractedPINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
Luk, K. C., Kehm, V., Carroll, J., Zhang, B., O’Brien, P., Trojanowski, J. Q., & Lee, V. M.-Y. (2012) · Science · doi:10.1126/science.1227157 · Cited by 2,563
ER Tubules Mark Sites of Mitochondrial Division
Friedman, J. R., Lackner, L. L., West, M., DiBenedetto, J. R., Nunnari, J., & Voeltz, G. K. (2011) · Science · doi:10.1126/science.1207385 · Cited by 2,072
Matsuda, N., Sato, S., Shiba, K., Okatsu, K., Saisho, K., Gautier, C. A., Sou, Y.-S., Saiki, S., Kawajiri, S., Sato, F., et al. (2010) · Journal of Cell Biology · doi:10.1083/jcb.200910140 · Cited by 1,969
International Parkinson's Disease Genomics Consortium (IPDGC), Nalls, M. A., Parkinson's Study Group (PSG) Parkinson's Research: The Organized GENetics Initiative (PROGENI), 23andMe, GenePD, NeuroGenetics Research Consortium (NGRC), Hussman Institute of Human Genomics (HIHG), Investigator, T. A. J. D., (CHARGE), C. F. H. A. A. R. I. G. E., North American Brain Expression Consortium (NABEC), et al. (2014) · Nature Genetics · doi:10.1038/ng.3043 · Cited by 1,895
MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE
Schapira, A. H. V., Cooper, J. A. D., Dexter, D. T., Jenner, P. G., Clark, J. B., & MARSDEN, C. D. (1989) · The Lancet · doi:10.1016/s0140-6736(89)92366-0 · Cited by 1,757
Autophagosomes form at ER–mitochondria contact sites
Hamasaki, M., Furuta, N., Matsuda, A., Nezu, A., Yamamoto, A., Fujita, N., Oomori, H., Noda, T., Haraguchi, T., Hiraoka, Y., et al. (2013) · Nature · doi:10.1038/nature11910 · Cited by 1,683
Ubiquitin is phosphorylated by PINK1 to activate parkin
Koyano, F., Okatsu, K., Kosako, H., Tamura, Y., Go, E., Kimura, M., Kimura, Y., Tsuchiya, H., Yoshihara, H., Hirokawa, T., et al. (2014) · Nature · doi:10.1038/nature13392 · Cited by 1,477
Self-citationPINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria
Chen, Y., & Dorn, G. W. (2013) · Science · doi:10.1126/science.1231031 · Cited by 1,323
Cited by
Sorted by citations
Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States
Mattson, M. P., & Arumugam, T. V. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.05.011 · Cited by 1,242
Selective neuronal vulnerability in Parkinson disease
Surmeier, D. J., Obeso, J. A., & Halliday, G. M. (2017) · Nature Reviews Neuroscience · doi:10.1038/nrn.2016.178 · Cited by 1,116
The SH-SY5Y cell line in Parkinson’s disease research: a systematic review
Xicoy, H., Wieringa, B., & Martens, G. J. M. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0149-0 · Cited by 1,036
Lewy pathology in Parkinson’s disease consists of crowded organelles and lipid membranes
Shahmoradian, S. H., Lewis, A. J., Genoud, C., Hench, J., Moors, T. E., Navarro, P. P., Castaño‐Díez, D., Schweighauser, G., Graff-Meyer, A., Goldie, K. N., et al. (2019) · Nature Neuroscience · doi:10.1038/s41593-019-0423-2 · Cited by 1,010
Oxidative stress and Parkinson’s disease
Blesa, J., Trigo-Damas, I., Quiroga-Varela, A., & Jackson-Lewis, V. R. (2015) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2015.00091 · Cited by 878
Metadata
- Authors
- Ryan, B. J., Hoek, S., Fon, E. A., & Wade-Martins, R.
- Affiliations
- University of Oxford (GB)
- Montreal Neurological Institute and Hospital (CA)
- Venue
- Trends in Biochemical Sciences
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 40
- Issue
- 4
- Pages
- 200-210
- ISSN
- 0968-0004 (ISSN-L)
- OpenAlex
- W2021439462
- Cited by
- 524
- References
- 115
- Citations by year
- 2026: 25 · 2025: 30 · 2024: 37 · 2023: 28 · 2022: 45 · 2021: 65 · 2020: 56 · 2019: 50 · 2018: 63 · 2017: 53 · 2016: 52 · 2015: 20
- FWCI
- 8.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Biochemical Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Parkinson's UK (J-0901)
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, mitochondrial dysfunction, mitophagy, PINK1, Parkin, alpha-synuclein, LRRK2, dopaminergic neurons, familial Parkinson's disease, sporadic Parkinson's disease, neurodegeneration, treatment options
- MeSH terms
- Animals, Humans, Mitochondria, Parkinson Disease, alpha-Synuclein
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