ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
The role of the mitochondrial protein VDAC1 in inflammatory bowel disease: a potential therapeutic target.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. 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 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of key mitochondria-related genes in necrotizing enterocolitis using single-cell hdWGCNA and experimental verification.Pediatric research · 2026Article
- The NLRP3 inflammasome as a dynamic context-dependent regulator: mechanisms, disease progression, and therapeutic implications.Journal of translational medicine · 2026Review
- Mitochondrial Dysfunction in Ulcerative Colitis: Pathogenic Mechanisms and Novel Therapeutics.Journal of biochemical and molecular toxicology · 2026Review
- Self-assembled nanoparticles from Xiexin Decoction attenuate ulcerative colitis by targeting VDAC1-Mediated NLRP3 inflammasome activation.Materials today. Bio · 2026Article
- Mitochondrial Calcium Overload Drives mtDNA-cGAS-STING Activation via VDAC1 and MCU Upregulation in Periodontitis.International journal of molecular sciences · 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
- Clotting the Gap Between Mitochondria-Mediated Immunity and Mitochondrial Transfer.Circulation research · 2026Review
- DIDS modulates VDAC1 oligomerization to suppress intrinsic apoptosis and attenuatesJournal of virology · 2026Article
- Mitochondrial DNA release via VDAC1 in keratinocytes: a key driver of innate immunity and vitiligo pathogenesis.Cell death & disease · 2026Article
- Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.Skin health and disease · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- Nitric oxide induces apoptosis of human primary melanocytes by regulating calcium homeostasis via VDAC1.Molecular and cellular biochemistry · 2025Article
- Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- VDAC1 as prognostic marker and therapeutic target in lung adenocarcinoma: a study integrating bioinformatics and experimental validation.Discover oncology · 2025Article
- MPTP mediated Ox-mtDNA release inducing macrophage pyroptosis and exacerbating MCD-induced MASH via promoting the ITPR3/CaJournal of translational medicine · 2025Article
- Effect of mitochondrial translocator protein TSPO on LPS-induced cardiac dysfunction.Journal of advanced research · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent studies have implicated mitochondrial dysfunction as a trigger of inflammatory bowel diseases, including Crohn's disease (CD) and ulcerative colitis (UC). We have investigated the role of the mitochondria gate-keeper protein, the voltage-dependent-anion channel 1 (VDAC1), in gastrointestinal inflammation and tested the effects of the newly developed VDAC1-interacting molecules, VBIT-4 and VBIT-12, on UC induced by dextran sulfate sodium (DSS) or trinitrobenzene sulphonic acid (TNBS) in mice. VDAC1, which controls metabolism, lipids transport, apoptosis, and inflammasome activation, is overexpressed in the colon of CD and UC patients and DSS-treated mice. VBIT-12 treatment of cultured colon cells inhibited the DSS-induced VDAC1 overexpression, oligomerization, and apoptosis. In the DSS-treated mice, VBIT-12 suppressed weight loss, diarrhea, rectal bleeding, pro-inflammatory cytokine production, crypt and epithelial cell damage, and focal inflammation. VBIT-12 also inhibited the infiltration of inflammatory cells, apoptosis, mtDNA release, and activation of caspase-1 and NRLP3 inflammasome to reduce the inflammatory response. The levels of the ATP-gated P
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