ReviewOxidative medicine and cellular longevity2022
Role of Glial Cell-Derived Oxidative Stress in Blood-Brain Barrier Damage after Acute Ischemic Stroke.
Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Diabetes and postoperative cognitive dysfunction and delirium in adults: mechanisms, biomarkers, and clinical management.Frontiers in endocrinology · 2026Review
- Protective effect and molecular mechanisms of magnolol in ischemic stroke.Pharmacological reports : PR · 2025Review
- The effects and mechanisms of stem cells and exosomes on neurological function protection and recovery after ischemic stroke.Neuroprotection (Chichester, England) · 2025Review
- Dynamic changes in BDNF, VEGF, and GDNF after transplanting human protein-based scaffolds with Wharton's Jelly MSCs in a rat brain injury model.Scientific reports · 2025Article
- Unlocking the therapeutic potential of tumor-derived EVs in ischemia-reperfusion: a breakthrough perspective from glioma and stroke.Journal of neuroinflammation · 2025Review
- Pharmacokinetics and Pharmacodynamics of a Nanostructured Lipid Carrier Co-Encapsulating Artemether and miRNA for Mitigating Cerebral Malaria.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Retracted: Role of Glial Cell-Derived Oxidative Stress in Blood-Brain Barrier Damage after Acute Ischemic Stroke.Oxidative medicine and cellular longevity · 2024Article
- Navigating neurological disorders: harnessing the power of natural compounds for innovative therapeutic breakthroughs.EXCLI journal · 2024Review
- ATP5J regulates microglial activation via mitochondrial dysfunction, exacerbating neuroinflammation in intracerebral hemorrhage.Frontiers in immunology · 2024Article
- Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.Aging and disease · 2023Review
- Ioversol Induced Microglia Proinflammatory Activation and Oxidative Stress in Rats.Neurotoxicity research · 2023Article
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
- Retraction · 2024-01-09Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The integrity of the blood-brain barrier (BBB) is mainly maintained by endothelial cells and basement membrane and could be regulated by pericytes, neurons, and glial cells including astrocytes, microglia, oligodendrocytes (OLs), and oligodendrocyte progenitor cells (OPCs). BBB damage is the main pathological basis of hemorrhage transformation (HT) and vasogenic edema after stroke. In addition, BBB damage-induced HT and vasogenic edema will aggravate the secondary brain tissue damage. Of note, after reperfusion, oxidative stress-initiated cascade plays a critical role in the BBB damage after acute ischemic stroke (AIS). Although endothelial cells are the target of oxidative stress, the role of glial cell-derived oxidative stress in BBB damage after AIS also should receive more attention. In the current review, we first introduce the physiology and pathophysiology of the BBB, then we summarize the possible mechanisms related to BBB damage after AIS. We aim to characterize the role of glial cell-derived oxidative stress in BBB damage after AIS and discuss the role of oxidative stress in astrocytes, microglia cells and oligodendrocytes in after AIS, respectively.
Indexed as
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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.