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
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1 retracted
TOM40 Mediates Mitochondrial Dysfunction Induced by α-Synuclein Accumulation in Parkinson’s Disease
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RetractedPINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
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MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE
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Autophagosomes form at ER–mitochondria contact sites
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Ubiquitin is phosphorylated by PINK1 to activate parkin
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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
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The beta-sitosterol beta-D-glucoside (BSSG) rat model of Parkinson's disease
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Serum Levels of the Parkinson's Disease-Linked Protein Parkin are Specifically Elevated in Covid-19Preprint
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Kumaree, K. K., Cheong, C. S. Y., Verma, K., Nadyani, K., Mahamud, N., Mahamad, P., Tencomnao, T., Prasansuklab, A., & Brimson, J. M. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27157004
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Mechanisms of lipid droplet-mitochondria interactions and their roles in diseases
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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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