The DOI matches its Crossref record; 233 of the 233 references it cites were found in a registry or an index.
VDAC1, mitochondrial dysfunction, and Alzheimer’s disease
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. Although an accumulation of brain amyloid-β (Aβ) peptide and hyperphosphorylated tau protein have been implicated in the pathogenesis of AD, the etiology of the disease remains unclear. Mitochondrial dysfunction has been identified as an early event in AD pathogenesis and is reflected by reduced metabolism, disruption of Ca 2+ homeostasis, and increased levels of reactive oxygen species, lipid peroxidation, and apoptosis. The focus of this review is the involvement of mitochondrial dysfunction in AD, and specifically, the role of the voltage-dependent anion channel 1 (VDAC1), which has been linked to AD pathogenesis. VDAC1 is a multi-functional protein, expressed in the mitochondria and other cell compartments, including the plasma membrane. The protein regulates the main metabolic and energetic functions of the cell, including Ca 2+ homeostasis, oxidative stress, and mitochondria-mediated apoptosis. VDAC1 represents a hub protein that interacts with over 150 other proteins including phosphorylated tau, Aβ, and γ-secretase, and participates in their toxicity. The high levels of VDAC1 demonstrated post-mortem in the brains of AD patients and in amyloid precursor protein (APP) transgenic mice prompted the hypothesis that the protein may be associated with neuronal cell destruction since over-expression of VDAC1 triggers cell death. Thus, targeting mitochondrial dysfunction via VDAC1, to prevent this pro-apoptotic activity, could represent a novel strategy for inhibiting cell death. In addition, the review also discusses possible VDAC1 involvement in the link between AD and diabetes and the inverse association between cancer and AD.
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“The voltage-dependent anion channel 1 (VDAC1), located in the outer mitochondrial membrane, regulates mitochondrial membrane permeability [94]”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [94]
In the citing paper
“A dynamic equilibrium between monomeric and oligomeric states of the protein exist, with the oligomeric state being formed upon apoptotic induction resulting in a channel through which cytochrome c efflux can occur [94].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [94]
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Research works printed but not linked: 1
- Shoshan-Barmatz, 2008, VDAC, the voltage-dependent anion channel: function, regulation & mitochondrial signaling in cell life and death, Cell Sci., 4, 74
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Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View
Cenini, G., Lloret, A., & Cascella, R. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/2105607 · Cited by 521
Kopp, K. O., Glotfelty, E. J., Li, Y., & Greig, N. H. (2022) · Pharmacological Research · doi:10.1016/j.phrs.2022.106550 · Cited by 298
Sphingolipids and lipid rafts: Novel concepts and methods of analysis
Bieberich, E. (2018) · Chemistry and Physics of Lipids · doi:10.1016/j.chemphyslip.2018.08.003 · Cited by 231
VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases
Shoshan‐Barmatz, V., Shteinfer‐Kuzmine, A., & Verma, A. (2020) · Biomolecules · doi:10.3390/biom10111485 · Cited by 246
Self-citationTang, K. S. (2019) · Life Sciences · doi:10.1016/j.lfs.2019.116695 · Cited by 223
Metadata
- Authors
- Shoshan-Barmatz, V., Nahon-Crystal, E., Shteinfer-Kuzmine, A., & Gupta, R.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- ORCID
- Gupta, Rajeev
- Venue
- Pharmacological Research
- Publisher
- Elsevier BV
- Published
- 2018-05
- Volume
- 131
- Pages
- 87-101
- ISSN
- 1043-6618 (ISSN-L)
- OpenAlex
- W2790842992
- Cited by
- 286
- References
- 233
- Citations by year
- 2026: 44 · 2025: 46 · 2024: 38 · 2023: 40 · 2022: 43 · 2021: 33 · 2020: 20 · 2019: 13 · 2018: 9
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pharmacological Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Phil and Sima Needleman Funds
- Israel Science Foundation (307/13)
- National Institute for Biotechnology in the Negev
- Ben-Gurion University
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, VDAC1, mitochondrial dysfunction, voltage-dependent anion channel, amyloid-beta, tau hyperphosphorylation, calcium homeostasis, oxidative stress, mitochondrial apoptosis, gamma-secretase, amyloid precursor protein, diabetes mellitus, cancer, neurodegeneration
- MeSH terms
- Alzheimer Disease, Animals, Calcium, Gene Expression Regulation, Humans, Mitochondria, Models, Molecular, Apoptosis, Voltage-Dependent Anion Channel 1, Protein Interaction Maps
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