ArticleActa biochimica et biophysica Sinica2024
AMPK/PGC-1α and p53 modulate VDAC1 expression mediated by reduced ATP level and metabolic oxidative stress in neuronal cells.
Article in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- T7 peptide-engineered liposomal Irisin mitigates PND progression through AMPK/PGC-1α signaling: multi-omic evidence of metabolic and epigenetic modulation.Journal of nanobiotechnology · 2026Article
- Mitochondrial protein-enriched artificial nanovesicles: mitochondrial recovery and antioxidation for diabetic wound treatment.Journal of nanobiotechnology · 2026Article
- TCMToxDB: a comprehensive database for the toxicological analysis of traditional Chinese medicines.Database : the journal of biological databases and curation · 2026Article
- p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.Biomolecules · 2026Article
- The Crosstalk Between Sepsis-Associated Encephalopathy and Alzheimer's Disease: Identifying Potential Biomarkers and Therapeutic Targets for Cognition.Molecular neurobiology · 2025Article
- The potential role of the SIRT1-Nrf2 signaling pathway in alleviating hidden hearing loss via antioxidant stress.Cell biology international · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-dependent anion channel 1 (VDAC1) is a pore protein located in the outer mitochondrial membrane. Its channel gating mediates mitochondrial respiration and cell metabolism, and it has been identified as a critical modulator of mitochondria-mediated apoptosis. In many diseases characterized by mitochondrial dysfunction, such as cancer and neurodegenerative diseases, VDAC1 is considered a promising potential therapeutic target. However, there is limited research on the regulatory factors involved in VDAC1 protein expression in both normal and pathological states. In this study, we find that VDAC1 protein expression is up-regulated in various neuronal cell lines in response to intracellular metabolic and oxidative stress. We further demonstrate that VDAC1 expression is modulated by intracellular ATP level. Through the use of pharmacological agonists and inhibitors and small interfering RNA (siRNA), we reveal that the AMPK/PGC-1α signaling pathway is involved in regulating VDAC1 expression. Additionally, based on bioinformatics predictions and biochemical verification, we identify p53 as a potential transcription factor that regulates
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