ReviewFrontiers in human neuroscience2017
White Matter Injury after Intracerebral Hemorrhage: Pathophysiology and Therapeutic Strategies.
Review in Frontiers in human neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Astrocyte-Microglia Crosstalk in Post-Hemorrhagic Neurovascular Microenvironment: Mechanistic Nodes, Cross-Stroke Comparisons, and Therapeutic Reprogramming.Translational stroke research · 2026Review
- Corticospinal tract risk modifies motor recovery after minimally invasive surgery for intracerebral hemorrhage: a secondary analysis of MISTIE-III.medRxiv : the preprint server for health sciences · 2026Article
- NDRG4 overexpression is associated with reduced apoptosis after intracerebral hemorrhage via the PI3K/Akt/GSK3β signaling pathway.Scientific reports · 2026Article
- Mesenchymal stem cell for hemorrhagic stroke: A clinical review.Regenerative therapy · 2025Review
- CXCR3-mediated natural killer cell infiltration exacerbates white matter injury after intracerebral haemorrhage.Brain : a journal of neurology · 2025Article
- Does low physical activity cause cognitive decline in elderly type 2 diabetes patients: A propensity score matching analysis.World journal of diabetes · 2025Article
- White Matter Injury in Central Nervous System Disorders.Neuropsychiatric disease and treatment · 2025Review
- Loss of microRNA-15a/16-1 function promotes neuropathological and functional recovery in experimental traumatic brain injury.JCI insight · 2024Article
- The Emerging Role of Microglial Hv1 as a Target for Immunomodulation in Myelin Repair.Aging and disease · 2024Review
- Unraveling the complex pathophysiology of white matter hemorrhage in intracerebral stroke: A single-cell RNA sequencing approach.CNS neuroscience & therapeutics · 2024Article
- Pretreated MSCs with IronQ Transplantation Attenuate Microglia Neuroinflammation via the cGAS-STING Signaling Pathway.Journal of inflammation research · 2024Article
- Piezo1 suppression reduces demyelination after intracerebral hemorrhage.Neural regeneration research · 2023Article
- Mesenchymal stem cells transplantation combined with IronQ attenuates ICH-induced inflammation response via Mincle/syk signaling pathway.Stem cell research & therapy · 2023Article
- Cyclophilin D-induced mitochondrial impairment confers axonal injury after intracerebral hemorrhage in mice.Neural regeneration research · 2023Article
- Secondary White Matter Injury Mediated by Neuroinflammation after Intracerebral Hemorrhage and Promising Therapeutic Strategies of Targeting the NLRP3 Inflammasome.Current neuropharmacology · 2023Review
- Preserving and enhancing mitochondrial function after stroke to protect and repair the neurovascular unit: novel opportunities for nanoparticle-based drug delivery.Frontiers in cellular neuroscience · 2023Review
- Prominent elevation of extracellular matrix molecules in intracerebral hemorrhage.Frontiers in molecular neuroscience · 2023Article
- Minocycline Alleviates White Matter Injury following Intracerebral Hemorrhage by Regulating CD4Oxidative medicine and cellular longevity · 2022Article
- Inflammation and immune cell abnormalities in intracranial aneurysm subarachnoid hemorrhage (SAH): Relevant signaling pathways and therapeutic strategies.Frontiers in immunology · 2022Review
- Intracerebral Hemorrhage: The Effects of Aging on Brain Injury.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) accounts for 10%-30% of all types of stroke. Bleeding within the brain parenchyma causes gray matter (GM) destruction as well as proximal or distal white matter (WM) injury (WMI) due to complex pathophysiological mechanisms. Because WM has a distinct cellular architecture, blood supply pattern and corresponding function, and its response to stroke may vary from that of GM, a better understanding of the characteristics of WMI following ICH is essential and may shed new light on treatment options. Current evidence using histological, radiological and chemical biomarkers clearly confirms the spatio-temporal distribution of WMI post- ICH. Although certain types of pathological damage such as inflammatory, oxidative and neuro-excitotoxic injury to WM have been identified, the exact molecular mechanisms remain unclear. In this review article, we briefly describe the constitution and physiological function of brain WM, summarize evidence regarding WMI, and focus on the underlying pathophysiological mechanisms and therapeutic strategies.
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