Neuron derived fractalkine promotes microglia to absorb hematoma via CD163/HO-1 after intracerebral hemorrhage

You, Mingfeng; Long, Chunnan; Wan, Yan; Guo, Hongxiu; Shen, Jing; Li, Man; He, Quanwei; Hu, Bo

doi:10.1007/s00018-022-04212-6

Cited by 13 publications

(13 citation statements)

References 44 publications

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“…In an isolated perfused rat heart model, the number of delayed remote ischemic preconditioning stimuli was positively correlated with HO-1, and HO-1 was involved in cardioprotection (41). As mentioned earlier, HO-1 levels are closely associated with hematoma clearance (28)(29)(30). Although the pathological mechanisms of ICH and cardiovascular disease are different, the relationship between RIC and HO-1 indicates interesting possibilities for future research.…”

Section: Remote Ischemic Conditioningmentioning

confidence: 82%

“…Although there is no logical connection between this and the findings of our research team, the significance between them necessitates further consideration. Similarly, the PPAR-γ pathway can enhance the expression of microglia CD163 and HO-1 as well as promote hematoma absorption (30); therefore, targeting HO-1 to promote hematoma absorption after ICH requires a combination of other molecules and multiple signaling pathways. In addition, further investigation is required into the therapeutic window of targeted HO-1, ideally in conjunction with its clinical application.…”

Section: Heme Oxygenasementioning

confidence: 99%

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Research progress of endogenous hematoma absorption after intracerebral hemorrhage

Zhang²,

Wu³

et al. 2023

Front. Neurol.

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Non-traumatic intraparenchymal brain hemorrhage is referred to as intracerebral hemorrhage (ICH). Although ICH is associated with a high rate of disability and case fatality, active intervention can significantly lower the rate of severe disability. Studies have shown that the speed of hematoma clearance after ICH determines the patient's prognosis. Following ICH, depending on the hematoma volume and mass effect, either surgical- or medication-only conservative treatment is chosen. The goal of promoting endogenous hematoma absorption is more relevant because surgery is only appropriate for a small percentage of patients, and open surgery can cause additional trauma to patients. The primary method of removing hematoma after ICH in the future will involve understanding how to produce and manage macrophage/microglial endogenous phagocytic hematomas. Therefore, it is necessary to elucidate the regulatory mechanisms and key targets for clinical purposes.

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Section: Remote Ischemic Conditioningmentioning

confidence: 82%

Section: Heme Oxygenasementioning

confidence: 99%

Research progress of endogenous hematoma absorption after intracerebral hemorrhage

Zhang²,

Wu³

et al. 2023

Front. Neurol.

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“…Gaetani first highlighted the expression of CX3CL1 and CX3CR1 in the human brain after ICH and TBI, finding that significant upregulation of CXC3L1/CXC3R1 might be involved in limiting brain damage ( Gaetani et al, 2013 ). You further speculated on the specific mechanism of CX3CL1 promoting hematoma clearance ( You et al, 2022 ). The expressions of both CX3CL1 and CX3CR1 increased early at 6 h of ICH onset, peaked at 3 days, and then decreased gradually in the following days.…”

Section: Chemokines and Their Receptors In Intracerebral Hemorrhagementioning

confidence: 99%

“…Interestingly, a study reported that the overexpression of CX3CR1 in adipose-derived stem cells promotes cell migration and functional recovery after experimental ICH, which might contribute to the development of stem cell therapy ( Li G. et al, 2019 ). Clinically, a prospective cohort including 30 ICH patients recently showed the relevance of serum CX3CL1 concentration and better prognosis ( You et al, 2022 ). Given the effects of CX3CL1 on hematoma absorption, it might be a promising target for ICH treatment in the ultra-early stage.…”

Section: Chemokines and Their Receptors In Intracerebral Hemorrhagementioning

confidence: 99%

The roles of chemokines following intracerebral hemorrhage in animal models and humans

Wang

Bian

et al. 2023

Front. Mol. Neurosci.

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Intracerebral hemorrhage (ICH) is one common yet devastating stroke subtype, imposing considerable burdens on families and society. Current guidelines are limited to symptomatic treatments after ICH, and the death rate remains significant in the acute stage. Thus, it is crucial to promote research to develop new targets on brain injury after ICH. In response to hematoma formation, amounts of chemokines are released in the brain, triggering the infiltration of resident immune cells in the brain and the chemotaxis of peripheral immune cells via the broken blood–brain barrier. During the past decades, mounting studies have focused on the roles of chemokines and their receptors in ICH injury. This review summarizes the latest advances in the study of chemokine functions in the ICH. First, we provide an overview of ICH epidemiology and underlying injury mechanisms in the pathogenesis of ICH. Second, we introduce the biology of chemokines and their receptors in brief. Third, we outline the roles of chemokines in ICH according to subgroups, including CCL2, CCL3, CCL5, CCL12, CCL17, CXCL8, CXCL12, and CX3CL1. Finally, we summarize current drug usage targeting chemokines in ICH and other cardio-cerebrovascular diseases. This review discusses the expressions of these chemokines and receptors under normal or hemorrhagic conditions and cell-specific sources. Above all, we highlight the related data of these chemokines in the progression and outcomes of the ICH disease in preclinical and clinical studies and point to therapeutic opportunities targeting chemokines productions and interactions in treating ICH, such as accelerating hematoma absorption and alleviating brain edema.

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“…CX3CR1 deficiency impairs microglial phagocytic clearance of neurotoxic species. Reportedly, CX3CL1 signaling enhances microglial erythrophagocytosis through the CD163/HO-1 axis ( 190 ), whereas CX3CR1 KO weakens microglial phagocytosis to β-amyloid and mediates lysosomal dysfunction, resulting in an escalation of neuroinflammation due to β-amyloid accumulation ( 191 ).…”

Section: Mechanisms Related To Inflammation In Rpmentioning

confidence: 99%

Neuroinflammation in retinitis pigmentosa: Therapies targeting the innate immune system

Ling

Hou²,

Yan³

2022

Front. Immunol.

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Retinitis pigmentosa (RP) is an important cause of irreversible blindness worldwide and lacks effective treatment strategies. Although mutations are the primary cause of RP, research over the past decades has shown that neuroinflammation is an important cause of RP progression. Due to the abnormal activation of immunity, continuous sterile inflammation results in neuron loss and structural destruction. Therapies targeting inflammation have shown their potential to attenuate photoreceptor degeneration in preclinical models. Regardless of variations in genetic background, inflammatory modulation is emerging as an important role in the treatment of RP. We summarize the evidence for the role of inflammation in RP and mention therapeutic strategies where available, focusing on the modulation of innate immune signals, including TNFα signaling, TLR signaling, NLRP3 inflammasome activation, chemokine signaling and JAK/STAT signaling. In addition, we describe epigenetic regulation, the gut microbiome and herbal agents as prospective treatment strategies for RP in recent advances.

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Neuron derived fractalkine promotes microglia to absorb hematoma via CD163/HO-1 after intracerebral hemorrhage

Cited by 13 publications

References 44 publications

Research progress of endogenous hematoma absorption after intracerebral hemorrhage

Research progress of endogenous hematoma absorption after intracerebral hemorrhage

The roles of chemokines following intracerebral hemorrhage in animal models and humans

Neuroinflammation in retinitis pigmentosa: Therapies targeting the innate immune system

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