ArticleScientific reports2020
VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 36 citations in OpenAlex.
- A membrane-disruptive action of VBIT-4 challenges its role as a widely used VDAC1 oligomerization inhibitor.eLife · 2026Article
- Multi-omics profiling of circulating proteins and metabolites in persistent atrial fibrillation: VDAC1 identified as a candidate circulating protein.International journal of cardiology. Heart & vasculature · 2026Article
- An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.Molecular & cellular proteomics : MCP · 2026Article
- Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases.Apoptosis : an international journal on programmed cell death · 2026Article
- Bioinformatics Analysis of Genes Associated with Autophagy and Metabolic Reprogramming in Atrial Fibrillation.Journal of cardiovascular development and disease · 2026Article
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- VBIT-4 Rescues Mitochondrial Dysfunction and Reduces Skeletal Muscle Degeneration in a Severe Model of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Article
- Mitochondrial proteins as biomarkers of cellular senescence and age-associated diseases.Aging · 2025Review
- A Membrane-Disruptive Action of VBIT-4 Challenges Its Role as a Widely Used VDAC Oligomerization Inhibitor.bioRxiv : the preprint server for biology · 2025Article
- Metformin-Induced Apoptosis Is Mediated Through Mitochondrial VDAC1.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Resveratrol's Pro-Apoptotic Effects in Cancer Are Mediated Through the Interaction and Oligomerization of the Mitochondrial VDAC1.International journal of molecular sciences · 2025Article
- Cardioprotective effect of Yiqi Huoxue decoction on post-myocardial infarction injury mediated by CaFrontiers in cardiovascular medicine · 2025Article
- Decoding Cancer through Silencing the Mitochondrial Gatekeeper VDAC1.Biomolecules · 2024Review
- Calcium signaling from sarcoplasmic reticulum and mitochondria contact sites in acute myocardial infarction.Journal of translational medicine · 2024Review
- VDAC in Retinal Health and Disease.Biomolecules · 2024Review
- Identification and validation of voltage-dependent anion channel 1-related genes and immune cell infiltration in diabetic nephropathy.Journal of diabetes investigation · 2024Article
- VDAC1 Protein Regulation of Oxidative Damage and Mitochondrial Dysfunction-Mediated Cytotoxicity by Silica Nanoparticles in SH-SY5Y Cells.Molecular neurobiology · 2023Article
- Apoptotic proteins with non-apoptotic activity: expression and function in cancer.Apoptosis : an international journal on programmed cell death · 2023Review
- Age-Dependent Changes in Calcium Regulation after Myocardial Ischemia-Reperfusion Injury.Biomedicines · 2023Article
- Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The voltage-dependent anion channel 1 (VDAC1) is a key player in mitochondrial function. VDAC1 serves as a gatekeeper mediating the fluxes of ions, nucleotides, and other metabolites across the outer mitochondrial membrane, as well as the release of apoptogenic proteins initiating apoptotic cell death. VBIT-4, a VDAC1 oligomerization inhibitor, was recently shown to prevent mitochondrial dysfunction and apoptosis, as validated in mouse models of lupus and type-2 diabetes. In the present study, we explored the expression of VDAC1 in the diseased myocardium of humans and rats. In addition, we evaluated the effect of VBIT-4 treatment on the atrial structural and electrical remodeling of rats exposed to excessive aldosterone levels. Immunohistochemical analysis of commercially available human cardiac tissues revealed marked overexpression of VDAC1 in post-myocardial infarction patients, as well as in patients with chronic ventricular dilatation\dysfunction. In agreement, rats exposed to myocardial infarction or to excessive aldosterone had a marked increase of VDAC1 in both ventricular and atrial tissues. Immunofluorescence staining indicated a punctuated appearance typical for mitochondrial-localized VDAC1. Finally, VBIT-4 treatment attenuated the atrial fibrotic load of rats exposed to excessive aldosterone without a notable effect on the susceptibility to atrial fibrillation episodes induced by burst pacing. Our results indicate that VDAC1 overexpression is associated with myocardial abnormalities in common pathological settings. Our data also indicate that inhibition of the VDAC1 can reduce excessive fibrosis in the atrial myocardium, a finding which may have important therapeutic implications. The exact mechanism\s of this beneficial effect need further studies.
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