ArticleJournal of neuroinflammation2020
Lipocalin 2 induces neuroinflammation and blood-brain barrier dysfunction through liver-brain axis in murine model of nonalcoholic steatohepatitis.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Analysis of Antimicrobial Peptide Expression Under Acute and Chronic Alcohol Exposure: A Cross-Sectional Study and a Systematic Review of the Literature.International journal of molecular sciences · 2026Pooled it
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- 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
- Hepatic and Brain Spatial Gene Expression Changes in Intragastric Alcohol Fed APP/PS1 Alzheimer's Disease Mouse Model.Research square · 2026Article
- Liver Organoids: From Disease Modelling to Regenerative Medicine.Cell proliferation · 2026Review
- Liver-derived complement component 3 promotes the susceptibility to stress-induced depression by impairing blood-brain barrier integrity.Molecular psychiatry · 2026Article
- Hepatokines lipocalin 2 and osteopontin drive muscle atrophy in MASH.Molecular metabolism · 2026Article
- The bone-cerebrovascular axis: effects of bone aging on neurovascular dysfunction and neurodegeneration.The Journal of clinical investigation · 2026Review
- Cyclin D1 regulates the hepatic response to feeding: Evidence for non-cell cycle roles in the liver.bioRxiv : the preprint server for biology · 2026Article
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- PD-1 Blockade-Induced DKK1 Expression by CD8+ T Cells Promotes Blood-Brain Barrier Permeabilization.Cancer discovery · 2026Article
- 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
- Diagnosis-specific associations of plasma NGAL in drug-naïve schizophrenia and major depressive disorder: an exploratory cross-sectional study.BMC psychiatry · 2026Article
- A microglial LCN2-MC4R signaling axis drives silica-induced neuronal damage via C1q release.Journal of neuroinflammation · 2026Article
- SHIV.D Infection Alters Production and Protein Composition of Myeloid-Derived Extracellular Vesicles.International journal of molecular sciences · 2026Article
- Article
- The liver-brain axis, from its function to preventive therapeutic strategies in diseases.Frontiers in endocrinology · 2026Review
- Neuroinflammation in Alzheimer's disease-associated sensory dysfunction: mechanistic links, actionable targets and therapeutic strategies.Frontiers in aging neuroscience · 2026Review
- Adriamycin nephropathy induces sensorineural hearing loss via blood-labyrinth barrier breakdown in BALB/c mice.Scientific reports · 2025Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRecent clinical and basic research implicated a strong correlation between NAFLD/NASH phenotypes with ectopic manifestations including neuroinflammation and neurodegeneration, but the mediators and critical pathways involved are not well understood. Lipocalin 2 (Lcn2) is one of the important mediators exclusively produced in the liver and circulation during NASH pathology.
methodsUsing murine model of NASH, we studied the role of Lcn2 as a potent mediator of neuroinflammation and neurodegeneration in NASH pathology via the liver-brain axis.
resultsResults showed that high circulatory Lcn2 activated 24p3R (Lipocalin2 receptor) in the brain and induced the release of high mobility group box 1 (HMGB1) preferably from brain cells. Released HMGB1 acted as a preferential ligand to toll-like receptor 4 (TLR4) and induced oxidative stress by activation of NOX-2 signaling involving activated p65 protein of the NF-κB complex. Further, the HMGB1-derived downstream signaling cascade activated NLRP3 inflammasome and release of proinflammatory cytokines IL-6 and IL-1β from brain cells. In addition, to advance our present understanding, in vitro studies were performed in primary brain endothelial cells where results showed high circulatory Lcn2 influenced HMGB1 secretion. Mechanistically, we also showed that elevated Lcn2 level in underlying NASH might be a likely cause for induction of blood-brain barrier dysfunction since the adipokine decreased the expression of tight junction protein Claudin 5 and caused subsequent elevation of pro-inflammatory cytokines IL-6 and IL-1β.
conclusionIn conclusion, the NASH-induced brain pathology might be because of increased Lcn2-induced release of HMGB1 and accompanying neuroinflammation.
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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.