ArticleCellular and molecular life sciences : CMLS2022
Neuron derived fractalkine promotes microglia to absorb hematoma via CD163/HO-1 after intracerebral hemorrhage.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Blood-brain barrier-penetrant nanotherapy inhibits haem oxygenase-1-mediated ferroptosis for post-resuscitation neuroprotection.Nature communications · 2026Article
- Neurovascular unit remodeling: focusing on glial cells in stroke injury and recovery.Frontiers in cellular neuroscience · 2026Review
- Advances in the multifunctional roles of CX3CL1 in the central nervous system.Frontiers in aging neuroscience · 2026Review
- Potential Therapeutic Targets and Emerging Strategies to Promote Hematoma Resolution in Intracerebral Hemorrhage.Revista de neurologia · 2025Review
- Hematoma Resorption in Intracerebral Hemorrhage: A Translational Overview on Pathophysiology, Biomarkers, and Innovative Therapies.Translational stroke research · 2025Review
- Clinical characteristics and outcomes of patients with traumatic brain injury transferred from ultra-high-altitude areas: patient series.Journal of neurosurgery. Case lessons · 2025Article
- Spi1 aggravates neuropathic pain by modulating Clec7a-mediated neuroinflammation and microglial phagocytosis.The journal of headache and pain · 2025Article
- New targets in spontaneous intracerebral hemorrhage.Current opinion in neurology · 2025Review
- Microglial Mechanisms and Therapeutic Potential in Brain Injury Post-Intracerebral Hemorrhage.Journal of inflammation research · 2025Review
- Gut microbiota depletion accelerates hematoma resolution and neurological recovery after intracerebral hemorrhage via p-coumaric acid-promoted Treg differentiation.Theranostics · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Fractalkine/CX3CR1 axis is critical for neuroprotection induced by hypoxic postconditioning against cerebral ischemic injury.Cell communication and signaling : CCS · 2024Article
- H3K9 trimethylation dictates neuronal ferroptosis through repressingJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- ACSL4-Mediated Ferroptosis and Its Potential Role in Central Nervous System Diseases and Injuries.International journal of molecular sciences · 2023Review
- Research progress of endogenous hematoma absorption after intracerebral hemorrhage.Frontiers in neurology · 2023Review
- The roles of chemokines following intracerebral hemorrhage in animal models and humans.Frontiers in molecular neuroscience · 2022Review
- Neuroinflammation in retinitis pigmentosa: Therapies targeting the innate immune system.Frontiers in immunology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHematoma leads to progressive neurological deficits and poor outcomes after intracerebral hemorrhage (ICH). Early clearance of hematoma is widely recognized as an essential treatment to limit the damage and improve the clinical prognosis. CD163, alias hemoglobin (Hb) scavenger receptor on microglia, plays a pivotal role in hematoma absorption, but CD163 on neurons permits Hb uptake and results in neurotoxicity. In this study, we focus on how to specially promote microglial but not neuronal CD163 mediated-Hb uptake and hematoma absorption.
methodsRNA sequencing was used to explore the potential molecules involved in ICH progression, and hematoma was detected by magnetic resonance imaging (MRI). Western blot and immunofluorescence were used to evaluate the expression and location of fractalkine (FKN) after ICH. Erythrophagocytosis assay was performed to study the specific mechanism of action of FKN in hematoma clearance. Small interfering RNA (siRNA) transfection was used to explore the effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) on hematoma absorption. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum FKN concentration in ICH patients.
resultsFKN was found to be significantly increased around the hematoma in a mouse model after ICH. With its unique receptor CX3CR1 in microglia, FKN significantly decreased the hematoma size and Hb content, and improved neurological deficits in vivo. Further, FKN could enhance erythrophagocytosis of microglia in vitro via the CD163/ hemeoxygenase-1 (HO-1) axis, while AZD8797 (a specific CX3CR1 inhibitor) reversed this effect. Moreover, PPAR-γ was found to mediate the increase in the CD163/HO-1 axis expression and erythrophagocytosis induced by FKN in microglia. Of note, a higher serum FKN level was found to be associated with better hematoma resolution in ICH patients.
conclusionsWe systematically identified that FKN may be a potential therapeutic target to improve hematoma absorption and we shed light on ICH treatment.
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