ReviewMetabolic brain disease2025
Oxytocin-mediated neuroprotection in ischemic stroke: molecular mechanisms, therapeutic potential and clinical translational prospects.
Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- An Epigenetic Switch for Sex-Specific Brain Resilience in Stroke: Targeting HDAC2 to Amplify Endogenous Oxytocin Signaling.ACS central science · 2026Article
- Resveratrol attenuates pyroptosis and neuroinflammation by inhibiting the TLR4/NF-κB/AIM2 pathway in ischemic stroke rats.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke (IS), also known as ischemic cerebrovascular accident, is a serious consequence of cerebral ischemia characterized by high morbidity, disability, and mortality. The primary causes of IS include atherosclerosis, cardiogenic embolism, large artery occlusion, and small artery disease. The occurrence of IS involves multiple cellular death mechanisms such as vascular obstruction, inflammatory response, excitotoxicity, oxidative stress, as well as neuronal apoptosis, necroptosis, and pyroptosis. Despite the application of current drugs and therapeutic strategies in the treatment of IS, their efficacy remains limited, and they are often accompanied by adverse effects. Therefore, identifying novel and more effective treatment strategies is of critical importance. In recent years, oxytocin (OT) has attracted widespread attention due to its multiple biological effects in the central nervous system, especially its neuroprotective effects. OT can reduce ischemic damage by stabilizing the blood-brain barrier (BBB), inhibiting neuroinflammation, alleviating oxidative stress, regulating excitotoxicity, and calcium overload. Additionally, OT promotes neurovascular remodeling via the VEGF/BDNF axis and modulates Na⁺/K⁺-ATPase activity, GABA signaling pathways, and DNA methylation, thereby contributing to recovery after stroke. However, the pharmacokinetic characteristics of OT, limitations in delivery methods, and the challenges of individualized treatment restrict its clinical application. This review will summarize the mechanisms of OT in IS, discuss the challenges and limitations in its clinical application, and explore future development directions, including optimization of nasal delivery systems, development of nanodrug carriers, use of perfusion-weighted imaging to determine the therapeutic window, and personalized treatment strategies based on genetic profiling. The aim is to provide theoretical support and guidance for further research on OT and its clinical application.
Indexed as
Identifiers
41264126What Socratic 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 Socratic graph.