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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 |
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creator | Akamatsu, Yosuke Pagan, Vicente A. Hanafy, Khalid A. |
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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