ArticleJournal of neuroinflammation2019
Poldip2 mediates blood-brain barrier disruption in a model of sepsis-associated encephalopathy.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Factors contributing to sepsis-associated encephalopathy: a comprehensive systematic review and meta-analysis.Frontiers in medicine · 2024Pooled it
- A multistage micro-nano biosystem prevents sepsis-associated encephalopathy through coordinated neuroinflammation suppression and gut-brain axis modulation.Bioactive materials · 2026Article
- Hydrogen alleviates sepsis-associated encephalopathy via ATG9B-dependent mitophagy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Fenofibrate alleviates the brain edema after traumatic brain injury by enhancing endothelial OXPHOS.Redox biology · 2026Article
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Recombinant TsP53 mitigates inflammation and blood-brain barrier disruption in CLP-induced septic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Mitochondrial dysfunction, neuroinflammation, and associated mechanisms in sepsis-associated encephalopathy: from pathogenesis to emerging therapeutics.Frontiers in neuroscience · 2026Review
- Article
- Unveiling the Role of LncRNA in Sepsis-Associated Encephalopathy.Current medical science · 2025Review
- Enterococcus-derived cytolysin exacerbates ischemic stroke by disrupting the blood-brain barrier via NLRP3 activation.Journal of neuroinflammation · 2025Article
- The Crosstalk Between Sepsis-Associated Encephalopathy and Alzheimer's Disease: Identifying Potential Biomarkers and Therapeutic Targets for Cognition.Molecular neurobiology · 2025Article
- The role of microglia in sepsis-associated encephalopathy: a narrative review.Translational pediatrics · 2025Review
- Protein lipoylation in cancer: metabolic reprogramming and therapeutic potential.Cell death discovery · 2025Review
- Dihydromyricetin protects hippocampal neurons in sepsis-associated encephalopathy by reducing ER stress-mediated apoptosis and inflammation.Journal of molecular histology · 2025Article
- OTUD1 exacerbates sepsis-associated encephalopathy by promoting HK2 mitochondrial release to drive microglia pyroptosis.Journal of neuroinflammation · 2025Article
- The hexapeptide functionalized gold nanoparticles protect against sepsis-associated encephalopathy by forming specific protein corona and regulating macrophage activation.Materials today. Bio · 2025Article
- Microglial NLRP3-gasdermin D activation impairs blood-brain barrier integrity through interleukin-1β-independent neutrophil chemotaxis upon peripheral inflammation in mice.Nature communications · 2025Article
- Polymerase delta-interacting protein 2 mediates brain vascular permeability by regulating ROS-mediated ZO-1 phosphorylation and localization at the interendothelial border.Cell communication and signaling : CCS · 2025Article
- Intestinal ischemia-reperfusion and blood-brain barrier compromise: pathways to cognitive dysfunction.Frontiers in neuroscience · 2025Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSepsis-associated encephalopathy (SAE), a diffuse cerebral dysfunction in the absence of direct CNS infection, is associated with increased rates of mortality and morbidity in patients with sepsis. Increased cytokine production and disruption of the blood-brain barrier (BBB) are implicated in the pathogenesis of SAE. The induction of pro-inflammatory mediators is driven, in part, by activation of NF-κΒ. Lipopolysaccharide (LPS), an endotoxin produced by gram-negative bacteria, potently activates NF-κΒ and its downstream targets, including cyclooxygenase-2 (Cox-2). Cox-2 catalyzes prostaglandin synthesis and in the brain prostaglandin, E2 is capable of inducing endothelial permeability. Depletion of polymerase δ-interacting protein 2 (Poldip2) has previously been reported to attenuate BBB disruption, possibly via regulation of NF-κΒ, in response to ischemic stroke. Here we investigated Poldip2 as a novel regulator of NF-κΒ/cyclooxygenase-2 signaling in an LPS model of SAE.
methodsIntraperitoneal injections of LPS (18 mg/kg) were used to induce BBB disruption in Poldip2
resultsHeterozygous deletion of Poldip2 conferred protection against LPS-induced BBB permeability. Alterations in Poldip2
conclusionsThese data suggest Poldip2 mediates LPS-induced BBB disruption by regulating NF-κΒ subunit p65 activation and Cox-2 and prostaglandin E2 induction. Consequently, targeted inhibition of Poldip2 may provide clinical benefit in the prevention of sepsis-induced BBB disruption.
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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.