An Update On Medical Treatment for Intracerebral Hemorrhage

Li, Xiang; Feng, Dongxia; Chen, Gang

doi:10.1007/s12975-018-0664-5

Cited by 11 publications

(11 citation statements)

References 102 publications

(108 reference statements)

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“…TLRs play key roles in immune and inflammatory responses to ICH [ 43 ]. TLR4 is known to be activated by hematoma components and induce neuroinflammation following ICH [ 44 ]. TLR4 also mediated hemorrhagic transformation following delayed tPA administration in experimental ischemic stroke [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

“…TNFAIP8 (TNF alpha-induced protein 8), a negative mediator of apoptosis [ 101 ], and HMGB1 also correlated with rPHE. HMGB1 is released by microglia following cell injury and death [ 102 ], and participates in ICH-induced inflammatory injury [ 44 ]. An HMGB-1 inhibitor attenuates ICH-induced injury in experimental ICH [ 102 , 103 ].…”

Section: Discussionmentioning

confidence: 99%

“…S1,S2). The NLRP3 inflammasome amplifies inflammatory ICH responses, with NLRP3 inhibitor MCC950 being administered as an ICH treatment [44,[49][50][51][52]. NLRP3 knock-down after ICH reduced brain edema and improved neurological outcomes [51].…”

Section: Genes/modules Associated With Ich and Aphe Volumesmentioning

confidence: 99%

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Molecular Correlates of Hemorrhage and Edema Volumes Following Human Intracerebral Hemorrhage Implicate Inflammation, Autophagy, mRNA Splicing, and T Cell Receptor Signaling

Durocher

Knepp

Yee

et al. 2020

Transl. Stroke Res.

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Intracerebral hemorrhage (ICH) and perihematomal edema (PHE) volumes are major determinants of ICH outcomes as is the immune system which plays a significant role in damage and repair. Thus, we performed whole-transcriptome analyses of 18 ICH patients to delineate peripheral blood genes and networks associated with ICH volume, absolute perihematomal edema (aPHE) volume, and relative PHE (aPHE/ICH; rPHE). We found 440, 266, and 391 genes correlated with ICH and aPHE volumes and rPHE, respectively (p < 0.005, partial-correlation > |0.6|). These mainly represented inflammatory pathways including NF-κB, TREM1, and Neuroinflammation Signaling—most activated with larger volumes. Weighted Gene Co-Expression Network Analysis identified seven modules significantly correlated with these measures (p < 0.05). Most modules were enriched in neutrophil, monocyte, erythroblast, and/or T cell-specific genes. Autophagy, apoptosis, HIF-1α, inflammatory and neuroinflammatory response (including Toll-like receptors), cell adhesion (including MMP9), platelet activation, T cell receptor signaling, and mRNA splicing were represented in these modules (FDR p < 0.05). Module hub genes, potential master regulators, were enriched in neutrophil-specific genes in three modules. Hub genes included NCF2, NCF4, STX3, and CSF3R, and involved immune response, autophagy, and neutrophil chemotaxis. One module that correlated negatively with ICH volume correlated positively with rPHE. Its genes and hubs were enriched in T cell-specific genes including hubs LCK and ITK, Src family tyrosine kinases whose modulation improved outcomes and reduced BBB dysfunction following experimental ICH. This study uncovers molecular underpinnings associated with ICH and PHE volumes and pathophysiology in human ICH, where knowledge is scarce. The identified pathways and hub genes may represent novel therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Molecular Correlates of Hemorrhage and Edema Volumes Following Human Intracerebral Hemorrhage Implicate Inflammation, Autophagy, mRNA Splicing, and T Cell Receptor Signaling

Durocher

Knepp

Yee

et al. 2020

Transl. Stroke Res.

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“…Some studies have shown that isoliquiritigenin, luteolin, and melatonin can modulate this signaling pathway [143][144][145]. Clinical trials have been performed addressing all the aspects above, but the results are insufficient [7].…”

Section: Potential Therapeutic Targets For Ich Based On the Frameworkmentioning

confidence: 99%

“…As the deadliest subtype of hemorrhagic stroke, intracerebral hemorrhage (ICH) accounts for 15% of all strokes worldwide and ranges from 20 to 30% in Asia, therefore seriously threatening human health worldwide [4][5][6]. Although a variety of drugs have been validated to exert effective neuroprotection in experimental ICH animal models in recent years, almost all of these drugs have performed poorly in clinical trials and have failed to achieve definite clinical efficacy for ICH [7][8][9][10][11][12][13][14][15][16][17][18][19]. The clinical trials are listed in Table 1.…”

Section: Introductionmentioning

confidence: 99%

Neurovascular Units and Neural-Glia Networks in Intracerebral Hemorrhage: from Mechanisms to Translation

Sun

Wang

et al. 2021

Transl. Stroke Res.

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Intracerebral hemorrhage (ICH), the most lethal type of stroke, often leads to poor outcomes in the clinic. Due to the complex mechanisms and cell-cell crosstalk during ICH, the neurovascular unit (NVU) was proposed to serve as a promising therapeutic target for ICH research. This review aims to summarize the development of pathophysiological shifts in the NVU and neural-glia networks after ICH. In addition, potential targets for ICH therapy are discussed in this review. Beyond cerebral blood flow, the NVU also plays an important role in protecting neurons, maintaining central nervous system (CNS) homeostasis, coordinating neuronal activity among supporting cells, forming and maintaining the blood-brain barrier (BBB), and regulating neuroimmune responses. During ICH, NVU dysfunction is induced, along with neuronal cell death, microglia and astrocyte activation, endothelial cell (EC) and tight junction (TJ) protein damage, and BBB disruption. In addition, it has been shown that certain targets and candidates can improve ICH-induced secondary brain injury based on an NVU and neural-glia framework. Moreover, therapeutic approaches and strategies for ICH are discussed.

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Genetically predicted hypotaurine levels mediate the relationship between immune cells and intracerebral hemorrhage

Cao,

Pi,

Zhang

et al. 2024

International Immunopharmacology

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An Update On Medical Treatment for Intracerebral Hemorrhage

Cited by 11 publications

References 102 publications

Molecular Correlates of Hemorrhage and Edema Volumes Following Human Intracerebral Hemorrhage Implicate Inflammation, Autophagy, mRNA Splicing, and T Cell Receptor Signaling

Molecular Correlates of Hemorrhage and Edema Volumes Following Human Intracerebral Hemorrhage Implicate Inflammation, Autophagy, mRNA Splicing, and T Cell Receptor Signaling

Neurovascular Units and Neural-Glia Networks in Intracerebral Hemorrhage: from Mechanisms to Translation

Genetically predicted hypotaurine levels mediate the relationship between immune cells and intracerebral hemorrhage

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