ReviewCurrent neuropharmacology2023
Secondary White Matter Injury Mediated by Neuroinflammation after Intracerebral Hemorrhage and Promising Therapeutic Strategies of Targeting the NLRP3 Inflammasome.
Review in Current neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- TIGAR overexpression alleviates intracerebral hemorrhage injury in mice by suppressing ATF4/NOX4/p22phox-mediated oxidative stress and inflammation.Acta pharmacologica Sinica · 2026Article
- Loss of Pericytic Integrin-β1 Exacerbates Blood-Brain Barrier Damage and Hemorrhagic Brain Injury.Stroke · 2026Article
- Failed resolution of inflammation in intracerebral haemorrhage.Nature reviews. Neurology · 2026Review
- The roles of microglia and astrocytes in inflammasomes and neurological disorders.Neural regeneration research · 2026Article
- CTSS regulates macrophage lipid metabolic reprogramming and white matter repair after intracerebral hemorrhage.Journal of translational medicine · 2026Article
- Dihydromyricetin (DHM) Inhibits Microglial Pyroptosis and Oxidative Stress After Spinal Cord Injury by Promoting STING-Mediated Autophagy.Biochemical genetics · 2026Article
- Chemobrain as a Neuroimmune Syndrome: Mechanisms, Modifiers, and Emerging Multi-Target Therapeutic Strategies.Molecules (Basel, Switzerland) · 2026Review
- Current Management of Resistant Hypertension in Patients with Intracerebral Hemorrhage.International journal of molecular sciences · 2026Review
- RIP1 Exacerbates BBB Disruption by Impairing Autophagy-Mediated A2 Astrocyte Polarization in Hypertension-Induced Cerebral Microhemorrhage in Mice.Neurochemical research · 2026Article
- Noni (Morinda citrifolia) and Neurodegeneration: Exploring its Role in Oxidative Stress, Neuroinflammation, and Cell Survival Pathways.Molecular neurobiology · 2025Review
- Microstructural brain changes and their impact on hemorrhagic stroke recovery: a neurite orientation dispersion and density imaging-based study.Quantitative imaging in medicine and surgery · 2025Article
- The Gut-Brain Axis in Brain Tumors: Insights into Tumor Development, Progression, and Therapy.Biomedicines · 2025Review
- Comprehensive insight on immune landscape in intracerebral hemorrhage patients with single-cell RNA sequencing: from blood to hematoma.Journal of neuroinflammation · 2025Article
- T cell receptor activation contributes to brain damage after intracerebral hemorrhage in mice.Journal of neuroinflammation · 2025Article
- White matter lesions contribute to motor and non-motor disorders in Parkinson's disease: a critical review.GeroScience · 2025Review
- Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage.Journal of inflammation research · 2025Review
- A new perspective on the regulation of neuroinflammation in intracerebral hemorrhage: mechanisms of NLRP3 inflammasome activation and therapeutic strategies.Frontiers in immunology · 2025Review
- Sphk1/S1P pathway promotes blood-brain barrier breakdown after intracerebral hemorrhage through inducing Nlrp3-mediated endothelial cell pyroptosis.Cell death & disease · 2024Article
- Cystatin C Attenuates Perihematomal Secondary Brain Injury by Inhibiting the Cathepsin B/NLRP3 Signaling Pathway in a Rat Model of Intracerebral Hemorrhage.Molecular neurobiology · 2024Article
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a neurological disease with high mortality and disability. Recent studies showed that white matter injury (WMI) plays an important role in motor dysfunction after ICH. WMI includes WMI proximal to the lesion and WMI distal to the lesion, such as corticospinal tract injury located at the cervical enlargement of the spinal cord after ICH. Previous studies have tended to focus only on gray matter (GM) injury after ICH, and fewer studies have paid attention to WMI, which may be one of the reasons for the poor outcome of previous drug treatments. Microglia and astrocyte-mediated neuroinflammation are significant mechanisms responsible for secondary WMI following ICH. The NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome activation, has been shown to exacerbate neuroinflammation and brain injury after ICH. Moreover, NLRP3 inflammasome is activated in microglia and astrocytes and exerts a vital role in microglia and astrocytes-mediated neuroinflammation. We speculate that NLRP3 inflammasome activation is closely related to the polarization of microglia and astrocytes and that NLRP3 inflammasome activation may exacerbate WMI by polarizing microglia and astrocytes to the pro-inflammatory phenotype after ICH, while NLRP3 inflammasome inhibition may attenuate WMI by polarizing microglia and astrocytes to the anti-inflammatory phenotype following ICH. Therefore, NLRP3 inflammasome may act as leveraged regulatory fulcrums for microglia and astrocytes polarization to modulate WMI and WM repair after ICH. This review summarized the possible mechanisms by which neuroinflammation mediated by NLRP3 inflammasome exacerbates secondary WMI after ICH and discussed the potential therapeutic targets.
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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.