ArticleInternational journal of molecular sciences2020
Neutralization of Lipocalin-2 Diminishes Stroke-Reperfusion Injury.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Anti-LCN2 antibody treatment is associated with attenuated hearing loss and blood-labyrinth barrier disruption in a mouse model of chronic kidney disease.Journal of molecular histology · 2026Article
- Hippocampal Lipocalin-2 in T2DM Associated Neurodegeneration: A Therapeutic Perspective.Neurochemical research · 2026Review
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Article
- Nrf2 Deficiency in Müller Cells Exacerbates Pathological Neovascularization in Ischemic Retinopathy.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Activity and Heterogeneity of Astrocytes in Neurological Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2025Review
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- Review
- Interaction Between Neutrophils and Elements of the Blood-Brain Barrier in the Context of Multiple Sclerosis and Ischemic Stroke.International journal of molecular sciences · 2025Review
- Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs.Bone research · 2025Review
- Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.Metabolic brain disease · 2025Article
- Role of lipocalin-2 in amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025Review
- Article
- Single-Cell Transcriptome Reveals Cell Type-Specific Molecular Pathology in a 2VO Cerebral Ischemic Mouse Model.Molecular neurobiology · 2024Article
- Aberrant activation of hippocampal astrocytes causes neuroinflammation and cognitive decline in mice.PLoS biology · 2024Article
- Lipocalin-2 as a prognostic marker in patients with acute exacerbation of idiopathic pulmonary fibrosis.Respiratory research · 2024Article
- Analysis of brain and blood single-cell transcriptomics in acute and subacute phases after experimental stroke.Nature immunology · 2024Article
- The interaction of lipocalin-2 and astrocytes in neuroinflammation: mechanisms and therapeutic application.Frontiers in immunology · 2024Review
- Effect of dexmedetomidine on ncRNA and mRNA profiles of cerebral ischemia-reperfusion injury in transient middle cerebral artery occlusion rats model.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Oxidative stress is a key contributor to the pathogenesis of stroke-reperfusion injury. Neuroinflammatory peptides released after ischemic stroke mediate reperfusion injury. Previous studies, including ours, have shown that lipocalin-2 (LCN2) is secreted in response to cerebral ischemia to promote reperfusion injury. Genetic deletion of LCN2 significantly reduces brain injury after stroke, suggesting that LCN2 is a mediator of reperfusion injury and a potential therapeutic target. Immunotherapy has the potential to harness neuroinflammatory responses and provides neuroprotection against stroke. Here we report that LCN2 was induced on the inner surface of cerebral endothelial cells, neutrophils, and astrocytes that gatekeep the blood-brain barrier (BBB) after stroke. LCN2 monoclonal antibody (mAb) specifically targeted LCN2 in vitro and in vivo, attenuating the induction of LCN2 and pro-inflammatory mediators (iNOS, IL-6, CCL2, and CCL9) after stroke. Administration of LCN2 mAb at 4 h after stroke significantly reduced neurological deficits, cerebral infarction, edema, BBB leakage, and infiltration of neutrophils. The binding epitope of LCN2 mAb was mapped to the β3 and β4 strands, which are responsible for maintaining the integrity of LCN2 cup-shaped structure. These data indicate that LCN2 can be pharmacologically targeted using a specific mAb to reduce reperfusion injury after stroke.
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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.