ArticleCellular and molecular life sciences : CMLS2020
Molecular mechanism of olesoxime-mediated neuroprotection through targeting α-synuclein interaction with mitochondrial VDAC.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- Dopaminergic Identity of SH-SY5Y Cells Across Differentiation Protocols in Parkinson's Disease Research: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Clinical potential and current progress of mesenchymal stem cells for Parkinson's disease: a systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Pooled it
- Mitochondrial Voltage-Dependent Anion Channel: From a Passive Pore to a Cellular Hub Through Protein Complexation.International journal of molecular sciences · 2026Review
- NDUFA4 Deletion Upregulates VDAC1 to Promote Mitochondrial Damage, Endoplasmic Reticulum Expansion, and Neuronal Apoptosis.Human mutation · 2026Article
- MiR-7 in neurological disorders: beyond metabolic dysregulation.Frontiers in neuroscience · 2026Review
- Hexokinase as a Central Hub in Neurodegeneration: From Metabolic Dysfunction to Therapeutic Innovation.Aging and disease · 2025Review
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Conformational plasticity of mitochondrial VDAC2 controls the kinetics of its interaction with cytosolic proteins.Science advances · 2025Article
- Global and local effects in lipid-mediated interactions between peripheral and integral membrane proteins.Frontiers in molecular biosciences · 2025Review
- VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.Biomolecules · 2024Review
- Review
- Therapeutic Implications and Regulations of Protein Post-translational Modifications in Parkinsons Disease.Cellular and molecular neurobiology · 2024Review
- Combining nano-differential scanning fluorimetry and microscale thermophoresis to investigate VDAC1 interaction with small molecules.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Gating of β-Barrel Protein Pores, Porins, and Channels: An Old Problem with New Facets.International journal of molecular sciences · 2023Review
- Multiple tethers of organelle contact sites are involved in α-synuclein toxicity in yeast.Molecular biology of the cell · 2023Article
- E as in Enigma: The Mysterious Role of the Voltage-Dependent Anion Channel Glutamate E73.International journal of molecular sciences · 2022Review
- Molecular and Cellular Interactions in Pathogenesis of Sporadic Parkinson Disease.International journal of molecular sciences · 2022Review
- Restricting α-synuclein transport into mitochondria by inhibition of α-synuclein-VDAC complexation as a potential therapeutic target for Parkinson's disease treatment.Cellular and molecular life sciences : CMLS · 2022Article
- VDAC1 regulates neuronal cell loss after retinal trauma injury by a mitochondria-independent pathway.Cell death & disease · 2022Article
- The Potential Role of Voltage-Dependent Anion Channel in the Treatment of Parkinson's Disease.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
An intrinsically disordered neuronal protein α-synuclein (αSyn) is known to cause mitochondrial dysfunction, contributing to loss of dopaminergic neurons in Parkinson's disease. Through yet poorly defined mechanisms, αSyn crosses mitochondrial outer membrane and targets respiratory complexes leading to bioenergetics defects. Here, using neuronally differentiated human cells overexpressing wild-type αSyn, we show that the major metabolite channel of the outer membrane, the voltage-dependent anion channel (VDAC), is a pathway for αSyn translocation into the mitochondria. Importantly, the neuroprotective cholesterol-like synthetic compound olesoxime inhibits this translocation. By applying complementary electrophysiological and biophysical approaches, we provide mechanistic insights into the interplay between αSyn, VDAC, and olesoxime. Our data suggest that olesoxime interacts with VDAC β-barrel at the lipid-protein interface thus hindering αSyn translocation through the VDAC pore and affecting VDAC voltage gating. We propose that targeting αSyn translocation through VDAC could represent a key mechanism for the development of new neuroprotective strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.