Parkinson's disease (PD) is a neurodegenerative disease second only to Alzheimer's disease in terms of prevalence. Previous studies have indicated that the occurrence and progression of PD are associated with mitochondrial dysfunction. Mitochondrial dysfunction is one of the most important causes for apoptosis of dopaminergic neurons. Therefore, maintaining the stability of mitochondrial functioning is a potential strategy in the treatment of PD. Voltage-dependent anion channel (VDAC) is the main component in the outer mitochondrial membrane, and it participates in a variety of biological processes. In this review, we focus on the potential roles of VDACs in the treatment of PD. We found that VDACs are involved in PD by regulating apoptosis, autophagy, and ferroptosis. VDAC1 oligomerization, VDACs ubiquitination, regulation of mitochondrial permeability transition pore (mPTP) by VDACs, and interaction between VDACs and α-synuclein (α-syn) are all promising methods for the treatment of PD. We proposed that inhibition of VDAC1 oligomerization and promotion of VDAC1 ubiquitination as an effective approach for the treatment of PD. Previous studies have proven that the expression of VDAC1 has a significant change in PD models. The expression levels of VDAC1 are decreased in the substantia nigra (SN) of patients suffering from PD compared with the control group consisting of normal individuals by using bioinformatics tools. VDAC2 is involved in PD mainly through the regulation of apoptosis. VDAC3 may have a similar function to VDAC1. It can be concluded that the functional roles of VDACs contribute to the therapeutic strategy of PD.
Copyright © 2022 Yajie He et al.