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

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 ha...

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Published in:Journal of neuroscience research 2020-03, Vol.98 (3), p.549-556
Main Authors: Akamatsu, Yosuke, Pagan, Vicente A., Hanafy, Khalid A.
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creator Akamatsu, Yosuke
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description 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.
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subjects adaptive immunity
Aneurysms
CD163
Cerebrospinal fluid
Circadian rhythms
Clinical trials
Cognitive ability
Heme
Heme‐Oxygenase
Hemorrhage
Inflammation
innate immunity
Macrophages
Microglia
Minireview
Oxygenase
Signal transduction
Stroke
Subarachnoid hemorrhage
TLR4 protein
toll like receptor
Toll-like receptors
Vasoconstriction
title The role of TLR4 and HO‐1 in neuroinflammation after subarachnoid hemorrhage
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