ReviewWorld journal of clinical cases2025
Role of nitric oxide in cerebral ischemia/reperfusion injury: A biomolecular overview.
Review in World journal of clinical cases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Therapeutic potential of nitric oxide and its donors in hemorrhagic and ischemic stroke: a systematic review.Medical gas research · 2026Pooled it
- Role of the Blood-Brain Barrier in the Pathophysiology of Major Depressive Disorder, Bipolar Disorder, and Schizophrenia: A Comparative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.Molecular neurobiology · 2026Review
- Therapeutic Gases in Biomedicine: Updates on Nitric Oxide and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Environmental Enrichment May Alleviate Neural Damage by Reducing Ferroptosis Through Tlr4.Molecular neurobiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is a gaseous molecule produced by 3 different NO synthase (NOS) isoforms: Neural/brain NOS (nNOS/bNOS, type 1), endothelial NOS (eNOS, type 3) and inducible NOS (type 2). Type 1 and 3 NOS are constitutively expressed. NO can serve different purposes: As a vasoactive molecule, as a neurotransmitter or as an immunomodulator. It plays a key role in cerebral ischemia/reperfusion injury (CIRI). Hypoxic episodes simulate the production of oxygen free radicals, leading to mitochondrial and phospholipid damage. Upon reperfusion, increased levels of oxygen trigger oxide synthases; whose products are associated with neuronal damage by promoting lipid peroxidation, nitrosylation and excitotoxicity. Molecular pathways in CIRI can be altered by NOS. Neuroprotective effects are observed with eNOS activity. While nNOS interplay is prone to endothelial inflammation, oxidative stress and apoptosis. Therefore, nNOS appears to be detrimental. The interaction between NO and other free radicals develops peroxynitrite; which is a cytotoxic agent. It plays a main role in the likelihood of hemorrhagic events by tissue plasminogen activator (t-PA). Peroxynitrite scavengers are currently being studied as potential targets to prevent hemorrhagic transformation in CIRI.
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Identifiers
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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.