ArticleCell death & disease2025
LCN2 induces neuronal loss and facilitates sepsis-associated cognitive impairments.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The core role of central nervous system in sepsis-related organ damage.Frontiers in immunology · 2025Pooled it
- Astrocytic LCN2 mediates pathological crosstalk with neurons to promote neuronal loss in sepsis-associated encephalopathy.Cell death and differentiation · 2026Article
- Roles of Lcn2 and neuroinflammation in a scopolamine-induced cognitive impairment animal model: implication of the NLRP3 inflammasome pathway.Genes & genomics · 2026Article
- Frontotemporal dementia associated CHCHD10Cell death & disease · 2026Article
- Impact of Chronic Mild Stress on Neurotrophic and Hypothalamic-Pituitary-Adrenal Factors in the Brain of Rats Submitted to Sepsis.Neurotoxicity research · 2026Article
- GBA1 F213I mutation increases the expression of LCN2 promoting neurodegeneration.Cell death and differentiation · 2026Article
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- From correlation to causation: cell-type-specific gene regulatory networks in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- RRx-001 ameliorates astrocyte pyroptosis by regulating LCN2-NLRP3 inflammasome activation in an MPTP-induced parkinson's disease mouse model.Cellular and molecular life sciences : CMLS · 2026Article
- Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026Review
- HLA DP/DRA molecule regulates systemic inflammation and neuroinflammation, aggravates cognitive impairment and long-term anxiety in murine model of sepsis-associated encephalopathy.Frontiers in immunology · 2026Article
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Down-regulation of lipocalin-2 alleviates depressive-like behaviors in mice through modulation of microglial activation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Identification and Analysis of Remimazolam's Potential Therapeutic Mechanisms in Murine Sepsis-Associated Encephalopathy via Transcriptomic Analysis.Journal of inflammation research · 2026Article
- Double-hit of MIA and Nod2 deficiency induces sex-specific offspring behavioral abnormalities through placental dysregulation.Translational psychiatry · 2025Article
- From Correlation to Causation: Cell-Type-Specific Gene Regulatory Networks in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Sepsis-associated encephalopathy (SAE) is a severe neurological syndrome marked by widespread brain dysfunctions due to sepsis. Despite increasing data supporting the hypothesis of neuronal damage, the exact mechanism of sepsis-related cognitive disorders and therapeutic strategies remain unclear and need further investigation. In this study, a sepsis model was established in C57 mice using lipopolysaccharide (LPS). The findings demonstrated that LPS exposure induced neuronal loss, synaptic and cognitive deficits accompanied by mitochondrial damage. Bioinformatics and western blot analyses demonstrated a significant increase in Lipocalin-2 (LCN2) during sepsis as a key hub gene involved in immune and neurological inflammation. Interestingly, the recombinant LCN2 protein exhibited similar effects on synaptic dysfunction and cognitive deficits in C57 mice. Conversely, downregulating LCN2 effectively nullified the impact of LPS, leading to the amelioration of synaptic and cognitive deficits, neuronal loss, and reactive oxygen species (ROS)-associated mitochondrial damage. These findings suggest a novel etiopathogenic mechanism of SAE, which is initiated by the increased LCN2, leading to neuronal loss and cognitive deficit. Inhibition of LCN2 could be therapeutically beneficial in treating sepsis-induced synaptic and cognitive impairments.
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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.