ArticleFrontiers in pharmacology2021
Pathological Neuroinflammatory Conversion of Reactive Astrocytes Is Induced by Microglia and Involves Chromatin Remodeling.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- IL-33 as a boundary-tissue state-transfer signal: a Reader-Alarmin-Effector architecture linking CNS and skin.Brain, behavior, & immunity - health · 2026Review
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- Article
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- "Stand by me": astrocyte-microglia crosstalk in central nervous system development, homeostasis, injury, and disease.Frontiers in network physiology · 2026Review
- Gut-derived small extracellular vesicles support trained innate immune tolerance in murine microglial cells.Frontiers in immunology · 2026Article
- Molecular components of the FPR2/ALX pathway participate in astrocyte-neuron resolution responses to afford maneb-induced toxicity.Cellular and molecular life sciences : CMLS · 2025Article
- Neuroinflammation-A Crucial Factor in the Pathophysiology of Depression-A Comprehensive Review.Biomolecules · 2025Review
- Epigenetic regulation-mediated disorders in dopamine transporter endocytosis: A novel mechanism for the pathogenesis of Parkinson's disease.Theranostics · 2025Review
- HDAC7 knockout mitigates astrocyte reactivity and neuroinflammation via the IRF3/cGAS/STING signaling pathway.Frontiers in cellular neuroscience · 2025Article
- Astrocyte epigenetics as a priority area in neuroscience research.Frontiers in molecular neuroscience · 2025Article
- Neuropsychiatric Manifestations of COVID-19 Disease and Post COVID Syndrome: The Role of N-acetylcysteine and Acetyl-L-carnitine.Current neuropharmacology · 2025Review
- Neuroprotective Effect of Flavonoid Agathisflavone in the Ex Vivo Cerebellar Slice Neonatal Ischemia.Molecules (Basel, Switzerland) · 2024Article
- A Biomimic Nanobullet with Ameliorative Inflammatory Microenvironment for Alzheimer's Disease Treatments.Advanced healthcare materials · 2024Article
- Astroglial Cells: Emerging Therapeutic Targets in the Management of Traumatic Brain Injury.Cells · 2024Review
- Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions.International journal of molecular sciences · 2023Review
- Sex-dependent factors of alcohol and neuroimmune mechanisms.Neurobiology of stress · 2023Article
- Neurodegeneration and inflammation crosstalk: Therapeutic targets and perspectives.IBRO neuroscience reports · 2023Article
- Reactive gliosis and neuroinflammation: prime suspects in the pathophysiology of post-acute neuroCOVID-19 syndrome.Frontiers in neurology · 2023Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following brain injury or in neurodegenerative diseases, astrocytes become reactive and may suffer pathological remodeling, features of which are the loss of their homeostatic functions and a pro-inflammatory gain of function that facilitates neurodegeneration. Pharmacological intervention to modulate this astroglial response and neuroinflammation is an interesting new therapeutic research strategy, but it still requires a deeper understanding of the underlying cellular and molecular mechanisms of the phenomenon. Based on the known microglial-astroglial interaction, the prominent role of the nuclear factor kappa B (NF-κB) pathway in mediating astroglial pathological pro-inflammatory gain of function, and its ability to recruit chromatin-remodeling enzymes, we first explored the microglial role in the initiation of astroglial pro-inflammatory conversion and then monitored the progression of epigenetic changes in the astrocytic chromatin. Different configurations of primary glial culture were used to modulate microglia-astrocyte crosstalk while inducing pro-inflammatory gain of function by lipopolysaccharide (LPS) exposure.
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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.