ReviewFrontiers in neuroscience2025
Mechanism of LCN2 in cerebral ischemia-reperfusion injury.
Review in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Sinomenine Liposomes Alleviate Neuropathic Pain in a Spared Nerve Injury Model by Regulating Astrocyte Reactivity Associated with Inhibition of the JAK2/STAT3 Pathway.Neurochemical research · 2026Article
- Exerkine-Mediated Regulation of the NLRP3 Inflammasome in Neuroprotection: Mechanistic Insights and the Role of Exercise.Molecular neurobiology · 2026Review
- Secondary demyelination after stroke: Glial cell crosstalk.IBRO neuroscience reports · 2026Review
- Molecularly self-assembled nanoplatforms for targeted ROS-scavenging and neuroinflammation alleviation in acute ischemic stroke.Materials today. Bio · 2026Article
- The effect of gentiopicroside on brain tissue repair in mice during the acute phase of middle cerebral artery occlusion.Molecular biology reports · 2026Article
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Jolkinolide B Mitigates Cerebral Ischemia-Reperfusion Injury by Promoting Microglial M1/M2 Polarization Through the JAK2/STAT3 Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- InceptionV4 and SEResNet101: precise predictors of intracranial hemorrhage and collateral circulation post-ischemic stroke intervention.Frontiers in neurology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process faced by brain tissues after ischemic stroke treatment, which involves mechanisms of inflammatory response, oxidative stress and apoptosis, and severely affects treatment outcome. Lipocalin-2 (LCN2), an acute-phase protein, is significantly up-regulated after CIRI and promotes neural repair by enhancing astrocyte phagocytosis, but its over-activation may also trigger secondary inflammation and demyelination injury. LCN2 also plays a key role in neuroinflammation regulation by regulating the polarization state of astrocytes and the release of inflammatory factors, and may affect the integrity of the blood-brain barrier and a variety of pathologic injury processes. In view of the important role of LCN2 in CIRI, this article reviews the mechanism of LCN2, aiming to provide new ideas and methods for the treatment of ischemic stroke.
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