ArticleCNS neuroscience & therapeutics2024
Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- White matter injury in neonatal rats is attenuated by GsMTx4 inhibiting oligodendrocyte precursor cell ferroptosis via the PIEZO1/GCLC signaling pathway.Pediatric research · 2026Article
- Phosphodiesterase 4 regulates pyroptosis in subarachnoid hemorrhage.Neural regeneration research · 2026Article
- VKORC1L1 Downregulation Induced Vitamin K Cycle Disorder Exacerbates Neuronal Ferroptosis After Spinal Cord Injury.Molecular neurobiology · 2026Article
- Hesperetin alleviates neuronal pyroptosis by promoting mitophagy via DHCR24/BACE1 signaling pathway after subarachnoid hemorrhage in mice.Apoptosis : an international journal on programmed cell death · 2026Article
- Gut Acetic Acid Alleviates Cognitive Impairment by Inhibiting Tau Hyperphosphorylation via Regulating FFAR3/Erk Pathway in Chronic Cerebral Ischemia Mice.Molecular neurobiology · 2025Article
- Microglia-Derived Exosomal miR-223-3p Targets the RhoB-NF-κB-CCL11 Axis in Astrocytes and Relieves Neuronal Damage in Subarachnoid Hemorrhage.Neurochemical research · 2025Article
- BDNF gene therapy rescues neuronal function via unique and common transcriptional responses in Aβ and tau-driven Alzheimer's disease mouse models.Biochemistry and biophysics reports · 2025Article
- Changes in 3D Chromatin Organization Drive Topologically Determined Gene Expression in the Poststroke Mouse Cortex.Stroke · 2025Article
- Exploration and practice of potential association prediction between diseases and drugs based on Swanson framework and bioinformatics.Scientific reports · 2024Article
- Rasd1 is involved in white matter injury through neuron-oligodendrocyte communication after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
aimsRasd1 has been reported to be correlated with neurotoxicity, metabolism, and rhythm, but its effect in case of subarachnoid hemorrhage (SAH) remained unclear. White matter injury (WMI) and ferroptosis participate in the early brain injury (EBI) after SAH. In this work, we have investigated whether Rasd1 can cause ferroptosis and contribute to SAH-induced WMI.
methodsLentivirus for Rasd1 knockdown/overexpression was administrated by intracerebroventricular (i.c.v) injection at 7 days before SAH induction. SAH grade, brain water content, short- and long-term neurobehavior, Western blot, real-time PCR, ELISA, biochemical estimation, immunofluorescence, diffusion tensor imaging (DTI), and transmission electron microscopy (TEM) were systematically performed. Additionally, genipin, a selective uncoupling protein 2(UCP2) inhibitor, was used in primary neuron and oligodendrocyte co-cultures for further in vitro mechanistic studies.
resultsRasd1 knockdown has improved the neurobehavior, glia polarization, oxidative stress, neuroinflammation, ferroptosis, and demyelination. Conversely, Rasd1 overexpression aggravated these changes by elevating the levels of reactive oxygen species (ROS), inflammatory cytokines, MDA, free iron, and NCOA4, as well as contributing to the decrease of the levels of UCP2, GPX4, ferritin, and GSH mechanistically. According to the in vitro study, Rasd1 can induce oligodendrocyte ferroptosis through inhibiting UCP2, increasing reactive oxygen species (ROS), and activating NCOA4-mediated ferritinophagy.
conclusionsIt can be concluded that Rasd1 exerts a modulated role in oligodendrocytes ferroptosis in WMI following SAH.
Indexed as
Identifiers
What OpenQuestion holds
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.