VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration

Voltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol. Mitochondrial dysfunction and oxidative stress...

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Main Authors: Shirel Argueti-Ostrovsky, Shir Barel, Joy Kahn, Adrian Israelson
Format: Article
Language:English
Published: MDPI AG 2024-12-01
Series:Biomolecules
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Online Access:https://www.mdpi.com/2218-273X/15/1/33
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author Shirel Argueti-Ostrovsky
Shir Barel
Joy Kahn
Adrian Israelson
author_facet Shirel Argueti-Ostrovsky
Shir Barel
Joy Kahn
Adrian Israelson
author_sort Shirel Argueti-Ostrovsky
collection DOAJ
description Voltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol. Mitochondrial dysfunction and oxidative stress are central features of neurodegenerative diseases. The pivotal functions of VDAC1 in controlling mitochondrial membrane permeability, regulating calcium balance, and facilitating programmed cell death pathways, position it as a key determinant in the delicate balance between neuronal viability and degeneration. Accordingly, increasing evidence suggests that VDAC1 is implicated in the pathophysiology of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and others. This review summarizes the current findings on the contribution of VDAC1 to neurodegeneration, focusing on its interactions with disease-specific proteins, such as amyloid-β, α-synuclein, and mutant SOD1. By unraveling the complex involvement of VDAC1 in neurodegenerative processes, this review highlights potential avenues for future research and drug development aimed at alleviating mitochondrial-related neurodegeneration.
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spelling doaj-art-c1433d05f6db423db3161c991c7afc922025-01-24T13:24:55ZengMDPI AGBiomolecules2218-273X2024-12-011513310.3390/biom15010033VDAC1: A Key Player in the Mitochondrial Landscape of NeurodegenerationShirel Argueti-Ostrovsky0Shir Barel1Joy Kahn2Adrian Israelson3Department of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, IsraelDepartment of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, IsraelDepartment of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, IsraelDepartment of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, IsraelVoltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol. Mitochondrial dysfunction and oxidative stress are central features of neurodegenerative diseases. The pivotal functions of VDAC1 in controlling mitochondrial membrane permeability, regulating calcium balance, and facilitating programmed cell death pathways, position it as a key determinant in the delicate balance between neuronal viability and degeneration. Accordingly, increasing evidence suggests that VDAC1 is implicated in the pathophysiology of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and others. This review summarizes the current findings on the contribution of VDAC1 to neurodegeneration, focusing on its interactions with disease-specific proteins, such as amyloid-β, α-synuclein, and mutant SOD1. By unraveling the complex involvement of VDAC1 in neurodegenerative processes, this review highlights potential avenues for future research and drug development aimed at alleviating mitochondrial-related neurodegeneration.https://www.mdpi.com/2218-273X/15/1/33VDAC1neurodegenerative diseasesALSParkinson’s diseaseAlzheimer’s disease
spellingShingle Shirel Argueti-Ostrovsky
Shir Barel
Joy Kahn
Adrian Israelson
VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
Biomolecules
VDAC1
neurodegenerative diseases
ALS
Parkinson’s disease
Alzheimer’s disease
title VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
title_full VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
title_fullStr VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
title_full_unstemmed VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
title_short VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration
title_sort vdac1 a key player in the mitochondrial landscape of neurodegeneration
topic VDAC1
neurodegenerative diseases
ALS
Parkinson’s disease
Alzheimer’s disease
url https://www.mdpi.com/2218-273X/15/1/33
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AT joykahn vdac1akeyplayerinthemitochondriallandscapeofneurodegeneration
AT adrianisraelson vdac1akeyplayerinthemitochondriallandscapeofneurodegeneration