ArticleJournal of neuroinflammation2022
Targeted BRD4 protein degradation by dBET1 ameliorates acute ischemic brain injury and improves functional outcomes associated with reduced neuroinflammation and oxidative stress and preservation of blood-brain barrier integrity.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Inflammatory biomarkers in cerebral venous thrombosis versus ischemic stroke: a network meta-analysis.Frontiers in neurology · 2025Pooled it
- BRD4 contributes to the cytokine-induced acquisition of an IL-13RA2-positive inflammatory fibroblast phenotype.Journal of Crohn's & colitis · 2026Article
- Eyes Toward the Clinic: Selective Inhibition and Degradation Approaches to Bromodomain-Containing Proteins.Chembiochem : a European journal of chemical biology · 2026Review
- Changes in Immune-Inflammation Status and Acute Ischemic Stroke Prognosis in Prospective Cohort.Annals of clinical and translational neurology · 2026Article
- Targeting epigenetic remodeling of the blood-brain barrier: current knowledge for drug therapy.Epigenomics · 2026Review
- Article
- Brd4 BD1 Domain Antagonism of MS436 Preserves Blood-Brain Barrier Integrity via Rnf43/β-Catenin Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Quercetin as a multifaceted neuroprotective agent against cerebral ischaemia-reperfusion injury: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Review
- BRD4 silencing attenuates hemin-induced neuronal ferroptosis and inflammation via the H3K27ac-ATF3 axis in an in vitro model of cerebral hemorrhage.European journal of medical research · 2025Article
- Myeloid SHP2 attenuates myocardial ischemia‑reperfusion injury via regulation of BRD4/SYK/STING/NOX4/NLRP3 signaling.Molecular medicine reports · 2025Article
- BRD4 Mediates Cadmium-Induced Oxidative Stress and Kidney Injury in Mice via Disruption of Redox Homeostasis.Toxics · 2025Article
- The Crucial Role of the Blood-Brain Barrier in Neurodegenerative Diseases: Mechanisms of Disruption and Therapeutic Implications.Journal of clinical medicine · 2025Review
- Effects of globalAging brain · 2025Article
- Electroacupuncture Improves Learning and Memory Impairment in Rats with Cerebral Ischemia/Reperfusion Injury by Promoting Microglia/Macrophage M2 Polarization Through Nrf2/HO-1 Pathway.Journal of inflammation research · 2025Article
- Uncovering a new mechanism of ischemic stroke: a study of the association between γδ T cells and immunoinflammation.Frontiers in immunology · 2025Review
- Stroke-induced neuroplasticity in spiny mice in the absence of tissue regeneration.NPJ Regenerative medicine · 2024Article
- Chemokines play a role in nerve damage and neuroprotection in vascular dementia.IBRO neuroscience reports · 2024Review
- Deciphering neuroprotective mechanism of nitroxoline in cerebral ischemia: network pharmacology and molecular modeling-based investigations.Molecular diversity · 2024Article
- Japanese encephalitis virus-induced DNA methylation contributes to blood-brain barrier permeability by modulating tight junction protein expression.Journal of neuroinflammation · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Bromodomain-containing protein 4 (BRD4), a member of the bromodomain and extra-terminal domain (BET) protein family, plays a crucial role in regulating inflammation and oxidative stress that are tightly related to stroke development and progression. Consequently, BRD4 blockade has attracted increasing interest for associated neurological diseases, including stroke. dBET1 is a novel and effective BRD4 degrader through the proteolysis-targeting chimera (PROTAC) strategy. We hypothesized that dBET1 protects against brain damage and neurological deficits in a transient focal ischemic stroke mouse model by reducing inflammation and oxidative stress and preserving the blood-brain barrier (BBB) integrity. Post-ischemic dBET1 treatment starting 4 h after stroke onset significantly ameliorated severe neurological deficits and reduced infarct volume 48 h after stroke. dBET1 markedly reduced inflammation and oxidative stress after stroke, indicated by multiple pro-inflammatory cytokines and chemokines including IL-1β, IL-6, TNF-α, CCL2, CXCL1 and CXCL10, and oxidative damage markers 4-hydroxynonenal (4-HNE) and gp91
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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.