ReviewFrontiers in molecular neuroscience2022
The role of lipocalin 2 in brain injury and recovery after ischemic and hemorrhagic stroke.
Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Secondary demyelination after stroke: Glial cell crosstalk.IBRO neuroscience reports · 2026Review
- Lipocalin-2 in Intracerebral Hemorrhage: Mechanisms, Biomarker Potential, and Therapeutic Targeting.Neuromolecular medicine · 2026Review
- Metabolic-dysfunction-associated steatohepatitis impairs cochlear integrity and delays auditory recovery after noise trauma.Cell communication and signaling : CCS · 2026Article
- Exploring Core Genes Involved in Ischemic Stroke and the Therapeutic Potential of Hyperbaric Oxygen: Insights from Transcriptomic Analysis.Neuromolecular medicine · 2025Article
- Astrocytes-derived LCN2 triggers EV-A71-induced muscle soreness via accumulating lactate.Science advances · 2025Article
- Plasma Neutrophil Gelatinase-Associated Lipocalin as a Biomarker of Kidney Injury and Potential Predictor of Hypoxic Brain Injury in Severe Plasmodium falciparum Malaria: Insights From India.Seminars in nephrology · 2025Review
- Identification of pivotal genes and regulatory networks associated with SAH based on multi-omics analysis and machine learning.Scientific reports · 2025Article
- Article
- Mechanism of LCN2 in cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2025Review
- Microglial Lcn2 knockout enhances chronic intracerebral hemorrhage recovery by restoring myelin and reducing inflammation.Theranostics · 2025Article
- The post-stroke young adult brain has limited capacity to re-express the gene expression patterns seen during early postnatal brain development.Brain pathology (Zurich, Switzerland) · 2024Article
- The Transcription Factor Ets1 Influences Axonal Growth via Regulation of Lcn2.Molecular neurobiology · 2024Article
- Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage.International journal of molecular sciences · 2023Review
- Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier.Frontiers in cellular neuroscience · 2023Article
- Lipocalin 2 receptors: facts, fictions, and myths.Frontiers in immunology · 2023Review
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Authors and funding
7 authors.
Funding
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Abstract
Ischemic and hemorrhagic stroke (including intracerebral hemorrhage, intraventricular hemorrhage, and subarachnoid hemorrhage) is the dominating cause of disability and death worldwide. Neuroinflammation, blood-brain barrier (BBB) disruption, neuronal death are the main pathological progress, which eventually causes brain injury. Increasing evidence indicated that lipocalin 2 (LCN2), a 25k-Da acute phase protein from the lipocalin superfamily, significantly increased immediately after the stroke and played a vital role in these events. Meanwhile, there exists a close relationship between LCN2 levels and the worse clinical outcome of patients with stroke. Further research revealed that LCN2 elimination is associated with reduced immune infiltrates, infarct volume, brain edema, BBB leakage, neuronal death, and neurological deficits. However, some studies revealed that LCN2 might also act as a beneficial factor in ischemic stroke. Nevertheless, the specific mechanism of LCN2 and its primary receptors (24p3R and megalin) involving in brain injury remains unclear. Therefore, it is necessary to investigate the mechanism of LCN2 induced brain damage after stroke. This review focuses on the role of LCN2 and its receptors in brain injury and aiming to find out possible therapeutic targets to reduce brain damage following stroke.
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