The role of TLR4 and HO-1 in neuroinflammation after subarachnoid hemorrhage

被引：41

作者：

Akamatsu, Yosuke ^{[1
]}

Pagan, Vicente A. ^{[2
]}

Hanafy, Khalid A. ^{[2
,3
]}

机构：

[1] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Neurosurg, Dept Surg, Boston, MA 02115 USA

[2] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02115 USA

[3] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Neurointens Care, 3 Blackfan Circle Rm 639, Boston, MA 02115 USA

来源：

JOURNAL OF NEUROSCIENCE RESEARCH | 2020年 / 98卷 / 03期

关键词：

adaptive immunity; CD163; Heme-Oxygenase; innate immunity; microglia; subarachnoid hemorrhage; toll like receptor; DELAYED CEREBRAL-ISCHEMIA; EARLY BRAIN-INJURY; HIGH-DOSE METHYLPREDNISOLONE; NECROSIS-FACTOR-ALPHA; K-CA CHANNELS; CARBON-MONOXIDE; DOUBLE-BLIND; SIGNALING PATHWAYS; VASOSPASM; RECEPTOR;

D O I：

10.1002/jnr.24515

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

This review on the mechanisms of neuroinflammation following subarachnoid hemorrhage will focus mainly on toll-like receptor 4 (TLR4), Heme Oxygenase-1 (HO-1), and the role of microglia and macrophages in this process. Vasospasm has long been the focus of research in SAH; however, clinical trials have shown that amelioration of vasospasm does not lead to an improved clinical outcome. This necessitates the need for novel avenues of research. Our work has demonstrated that microglial TLR4 and microglial HO-1, not only affects cognitive dysfunction, but also circadian dysrhythmia in a mouse model of SAH. To attempt to translate these findings, we have also begun investigating macrophages in the cerebrospinal fluid of SAH patients. The goal of this review is to provide an update on the role of TLR4, HO-1, and other signal transduction pathways in SAH-induced neuroinflammation.

引用

页码：549 / 556

页数：8

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