ArticleStroke2020
Prx2 (Peroxiredoxin 2) as a Cause of Hydrocephalus After Intraventricular Hemorrhage.
Article in Stroke, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- The Role of Peroxiredoxins in the Mechanisms of Oxidative Stress in Patients After Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2026Review
- Peroxiredoxins in Stroke: Friends and Foes.Cells · 2026Review
- Regulation of Choroid Plexus Bicarbonate Transporters Following Intraventricular Hemorrhage in Mice.Cell biochemistry and function · 2026Article
- Neutrophil Extracellular Traps Activate Meningeal Fibroblast to Aggravate Subarachnoid Fibrosis in Kaolin-Induced Hydrocephalus in Rats.Immunity, inflammation and disease · 2025Article
- Comprehensive transcriptomic analysis integrating bulk and single-cell RNA-seq with machine learning to identify and validate mitochondrial unfolded protein response biomarkers in patients with ischemic stroke.Frontiers in cell and developmental biology · 2025Article
- Mechanisms of hydrocephalus after intraventricular haemorrhage: a review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024Review
- Peroxiredoxin II exerts neuroprotective effects by inhibiting endoplasmic reticulum stress and oxidative stress-induced neuronal pyroptosis.Molecular biology reports · 2024Article
- Choroid plexus immune cell response in murine hydrocephalus induced by intraventricular hemorrhage.Fluids and barriers of the CNS · 2024Article
- Intracerebral hemorrhage-induced brain injury in mice: The role of peroxiredoxin 2-Toll-like receptor 4 inflammatory axis.CNS neuroscience & therapeutics · 2024Article
- Aquaporin 4 Mediates the Effect of Iron Overload on Hydrocephalus After Intraventricular Hemorrhage.Neurocritical care · 2024Article
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- Peroxiredoxin 2 Is a Potential Objective Indicator for Severity and the Clinical Status of Subarachnoid Hemorrhage Patients.Disease markers · 2023Article
- Therapeutic strategies to recover ependymal barrier after inflammatory damage: relevance for recovering neurogenesis during development.Frontiers in neuroscience · 2023Review
- The Fate of Erythrocytes after Cerebral Hemorrhage.Translational stroke research · 2022Review
- Posthemorrhagic hydrocephalus associates with elevated inflammation and CSF hypersecretion via activation of choroidal transporters.Fluids and barriers of the CNS · 2022Article
- Early Enteral Nutrition Can Reduce Incidence of Postoperative Hydrocephalus in Patients with Severe Hypertensive Intracerebral Hemorrhage.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review.Fluids and barriers of the CNS · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Background and Purpose- Our recent study demonstrated that release of Prx2 (peroxiredoxin 2) from red blood cells (RBCs) is involved in the inflammatory response and brain injury after intracerebral hemorrhage. The current study investigated the role of extracellular Prx2 in hydrocephalus development after experimental intraventricular hemorrhage. Methods- There were 4 parts in this study. First, Sprague-Dawley rats received an intraventricular injection of lysed RBC or saline and were euthanized at 1 hour for Prx2 measurements. Second, rats received an intraventricular injection of Prx2, deactivated Prx2, or saline. Third, lysed RBC was coinjected with conoidin A, a Prx2 inhibitor, or vehicle. Fourth, rats received Prx2 injection and were treated with minocycline or saline (i.p.). The effects of Prx2 and the inhibitors were examined using magnetic resonance imaging assessing ventriculomegaly, histology assessing ventricular wall damage, and immunohistochemistry to assess inflammation, particularly at the choroid plexus. Results- Intraventricular injection of lysed RBC resulted in increased brain Prx2 and hydrocephalus. Intraventricular injection of Prx2 alone caused hydrocephalus, ventricular wall damage, activation of choroid plexus epiplexus cells (macrophages), and an accumulation of neutrophils. Conoidin A attenuated lysed RBC-induced injury. Systemic minocycline treatment reduced the epiplexus cell activation and hydrocephalus induced by Prx2. Conclusions- Prx2 contributed to the intraventricular hemorrhage-induced hydrocephalus, probably by inducing inflammatory responses in choroid plexus and ventricular wall damage.
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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.