Abstract
Background: The Voltage Dependent Anion Channel (VDAC) proteins represent the most important pore-forming proteins of the mitochondrial outer membrane, directly involved in metabolism and apoptosis regulation. Literature has highlighted a key role of VDACs in mitochondrial dysfunction typical of many neurodegenerative disorders. In particular, the principal isoform VDAC1 represents the main mitochondrial docking site of many misfolded proteins, such as amyloid β and Tau in Alzheimer's disease, α-synuclein in Parkinson's disease and several SOD1 mutants in Amyotrophic Lateral Sclerosis. The interaction of misfolded proteins with VDAC1 has a strong impact on both cellular bioenergetics and apoptosis' pathways alteration. Therefore, VDACs represent a promising therapeutic target in neurodegeneration.
Objective: This review summarizes the roles of VDAC isoforms, and particularly of VDAC1, in the most common neurological disorders and analyzes in detail molecules and peptides available so far, able to interact and modulate VDAC1 in any considered pathological condition.
Conclusion: This review offers a description of the most promising therapeutic strategies acting on VDAC1, for the treatment of neurodegenerative diseases.
Keywords: VDAC, mitochondrial dysfunction, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis.
Current Medicinal Chemistry
Title:Interactions of VDAC with Proteins Involved in Neurodegenerative Aggregation: An Opportunity for Advancement on Therapeutic Molecules
Volume: 24 Issue: 40
Author(s): Andrea Magri*Angela Messina*
Affiliation:
- Department of Biological, Geological and Environmental Sciences, University of Catania, Catania,Italy
- Department of Biological, Geological and Environmental Sciences, University of Catania, Catania,Italy
Keywords: VDAC, mitochondrial dysfunction, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis.
Abstract: Background: The Voltage Dependent Anion Channel (VDAC) proteins represent the most important pore-forming proteins of the mitochondrial outer membrane, directly involved in metabolism and apoptosis regulation. Literature has highlighted a key role of VDACs in mitochondrial dysfunction typical of many neurodegenerative disorders. In particular, the principal isoform VDAC1 represents the main mitochondrial docking site of many misfolded proteins, such as amyloid β and Tau in Alzheimer's disease, α-synuclein in Parkinson's disease and several SOD1 mutants in Amyotrophic Lateral Sclerosis. The interaction of misfolded proteins with VDAC1 has a strong impact on both cellular bioenergetics and apoptosis' pathways alteration. Therefore, VDACs represent a promising therapeutic target in neurodegeneration.
Objective: This review summarizes the roles of VDAC isoforms, and particularly of VDAC1, in the most common neurological disorders and analyzes in detail molecules and peptides available so far, able to interact and modulate VDAC1 in any considered pathological condition.
Conclusion: This review offers a description of the most promising therapeutic strategies acting on VDAC1, for the treatment of neurodegenerative diseases.
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Cite this article as:
Magri Andrea *, Messina Angela *, Interactions of VDAC with Proteins Involved in Neurodegenerative Aggregation: An Opportunity for Advancement on Therapeutic Molecules, Current Medicinal Chemistry 2017; 24 (40) . https://dx.doi.org/10.2174/0929867324666170601073920
DOI https://dx.doi.org/10.2174/0929867324666170601073920 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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