ArticleJournal of neuroinflammation2017
Microglia-derived IL-1β contributes to axon development disorders and synaptic deficit through p38-MAPK signal pathway in septic neonatal rats.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 102 citations in OpenAlex.
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- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- Systemic Inflammation Triggers Motor Axon Degeneration Via Macrophage IL-1β-Mediated P53/SIRT1/Autophagy Pathway.Inflammation · 2026Article
- Metabolic Reprogramming Bridges Environmental Exposure and Tinnitus Severity: Evidence from AI-Driven Serum Multiomics.Environment & health (Washington, D.C.) · 2026Article
- NFE2L2 suppresses microglia-mediated neuroinflammation to preserve neuronal dendritic architecture from cadmium-induced damage.Cell biology and toxicology · 2026Article
- NADPH alleviates LPS-induced neuropathology and depression-like behaviors by suppressing microglial inflammatory response.Translational psychiatry · 2025Article
- Quantitative proteomic analysis of the brain reveals the potential antidepressant mechanism of Jiawei Danzhi Xiaoyao San in a chronic unpredictable mild stress mouse model of depression.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Anesthesia-induced developmental neurotoxicity in the setting of systemic inflammation: the role of microglia.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Biomarkers and therapeutic targets in early Alzheimer's disease: an Olink proteomics study.Frontiers in neurology · 2025Article
- The Biological Changes of Synaptic Plasticity in the Pathological Process of Sepsis-associated Encephalopathy.Current neuropharmacology · 2025Review
- Lethal versus surviving sepsis phenotypes displayed a partly differential regional expression of neurotransmitters and inflammation and did not modify the blood-brain barrier permeability in female CLP mice.Intensive care medicine experimental · 2024Article
- Article
- IL-1β, the first piece to the puzzle of sepsis-related cognitive impairment?Frontiers in neuroscience · 2024Review
- Exosomes Derived from M2 Microglial Cells Modulated by 1070-nm Light Improve Cognition in an Alzheimer's Disease Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Involvement of IL-1β-Mediated Necroptosis in Neurodevelopment Impairment after Neonatal Sepsis in Rats.International journal of molecular sciences · 2023Article
- Inhibition of p38 ameliorates axonal loss with modulation of autophagy in TNF-induced optic nerve damage.International ophthalmology · 2023Article
- Hydrogen sulfide-induced post-translational modification as a potential drug target.Genes & diseases · 2023Review
- Consequences of oxygen deprivation on myelination and sex-dependent alterations.Molecular and cellular neurosciences · 2023Review
- Asiaticoside Mitigates Alzheimer's Disease Pathology by Attenuating Inflammation and Enhancing Synaptic Function.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAxon development plays a pivotal role in the formation of synapse, nodes of Ranvier, and myelin sheath. Interleukin-1β (IL-1β) produced by microglia may cause myelination disturbances through suppression of oligodendrocyte progenitor cell maturation in the septic neonatal rats. Here, we explored if a microglia-derived IL-1β would disturb axon development in the corpus callosum (CC) following lipopolysaccharide (LPS) administration, and if so, whether it is associated with disorder of synapse formation in the cerebral cortex and node of Ranvier.
methodsSprague-Dawley rats (1-day old) in the septic model group were intraperitoneally administrated with lipopolysaccharide (1 mg/kg) and then sacrificed for detection of IL-1β, interleukin-1 receptor (IL-1R
resultsIn 1-day old septic rats, IL-1β expression was increased in microglia coupled with upregulated expression of IL-1R
conclusionsThe present results suggest that microglia-derived IL-1β might suppress axon development through activation of p38-MAPK signaling pathway that would contribute to formation disorder of cortical synapses and node of Ranvier following LPS exposure.
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