ArticleOxidative medicine and cellular longevity2020
VX765 Attenuates Pyroptosis and HMGB1/TLR4/NF-
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Research progress on microglial pyroptosis and inflammasomes: a comprehensive analysis.Frontiers in aging neuroscience · 2025Pooled it
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Exosomes from LPS-stimulated macrophages alleviate neuroinflammatory responses by reducing pyroptosis in systemic lipopolysaccharide-induced mice.Journal of applied biomedicine · 2025Article
- Neuroprotective Effects of the Nonsteroidal Anti-inflammatory Drug Celecoxib Against Caspase-1-dependent Pyroptosis Partially by Suppressing the HMGB1/TLR4 Pathway.Cellular and molecular neurobiology · 2025Article
- From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology.International journal of molecular sciences · 2025Review
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- Synthesizing network pharmacology, bioinformatics, and in vitro experimental verification to screen candidate targets of Salidroside for mitigating Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.Journal of neuroinflammation · 2025Review
- Propofol and remifentanil anesthesia improves cerebral oxygen balance and accelerates recovery in patients undergoing craniotomy for traumatic brain injury.American journal of translational research · 2025Article
- Targeting inflammasome pathway towards therapeutics of neurodegenerative diseases.Organelle (Tucson, Ariz.) · 2025Article
- Mitochondrial and ER stress crosstalk in TBI: mechanistic insights and therapeutic opportunities.Frontiers in cellular neuroscience · 2025Review
- Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.Burns & trauma · 2025Review
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- The dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions.MedComm · 2024Review
- Multi-regulatory potency of USP1 on inflammasome components promotes pyroptosis in thyroid follicular cells and contributes to the progression of Hashimoto's thyroiditis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- The roles of AIM2 in neurodegenerative diseases: insights and therapeutic implications.Frontiers in immunology · 2024Review
- Review
- Hypoxic preconditioned mesenchymal stem cells ameliorate rat brain injury after cardiopulmonary resuscitation by suppressing neuronal pyroptosis.Journal of cellular and molecular medicine · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic brain injury (TBI) refers to temporary or permanent damage to brain function caused by penetrating objects or blunt force trauma. TBI activates inflammasome-mediated pathways and other cell death pathways to remove inactive and damaged cells, however, they are also harmful to the central nervous system. The newly discovered cell death pattern termed pyroptosis has become an area of interest. It mainly relies on caspase-1-mediated pathways, leading to cell death.
methodsOur research focus is VX765, a known caspase-1 inhibitor which may offer neuroprotection after the process of TBI. We established a controlled cortical impact (CCI) mouse model and then controlled the degree of pyroptosis in TBI with VX765. The effects of caspase-1 inhibition on inflammatory response, pyroptosis, blood-brain barrier (BBB), apoptosis, and microglia activation, in addition to neurological deficits, were investigated.
resultsWe found that TBI led to NOD-like receptors (NLRs) as well as absent in melanoma 2 (AIM2) inflammasome-mediated pyroptosis in the damaged cerebral cortex. VX765 curbed the expressions of indispensable inflammatory subunits (caspase-1 as well as key downstream proinflammatory cytokines such as interleukin- (IL-) 1
conclusionIn conclusion, VX765 can counteract neurological damage after TBI by reducing pyroptosis and HMGB1/TLR4/NF-
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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.