Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation : A Systematic Review

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Ahmed , H , Khan , M A , Kahlert , U D , Niemela , M , Haenggi , D , Chaudhry , S R & Muhammad , S 2021 , ' Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation : A Systematic Review ' , International Journal of Molecular Sciences , vol. 22 , no. 8 , 4185 . https://doi.org/10.3390/ijms22084185

Title: Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation : A Systematic Review
Author: Ahmed, Hammad; Khan, Mahtab Ahmad; Kahlert, Ulf Dietrich; Niemela, Mika; Haenggi, Daniel; Chaudhry, Shafqat Rasul; Muhammad, Sajjad
Contributor organization: Department of Neurosciences
HUS Neurocenter
Neurokirurgian yksikkö
Clinicum
Date: 2021-04
Language: eng
Number of pages: 14
Belongs to series: International Journal of Molecular Sciences
ISSN: 1422-0067
DOI: https://doi.org/10.3390/ijms22084185
URI: http://hdl.handle.net/10138/331681
Abstract: Myeloid differentiation 88 (MyD88) is a well-established inflammatory adaptor protein. It is one of the essential downstream proteins of the toll-like receptor 4 (TLR4) signaling pathway. TLRs are pattern recognition receptors that are usually activated by the damage-associated molecular pattern molecules (DAMPs). Sterile inflammation is triggered by the endogenous DAMPs released in response to global cerebral ischemia and from extravasated blood after subarachnoid hemorrhage (SAH). In this review, we highlight the importance of the neuroinflammatory role of the MyD88 in the SAH. We also explore a few possible pharmacological agents that can be used to decrease SAH-associated neuroinflammation by modulating the MyD88 dependent functions. Pharmacological agents such as flavonoids, melatonin, fluoxetine, pentoxifylline and progesterone have been investigated experimentally to reduce the SAH-associated inflammation. Inhibition of the MyD88 not only reduces the expression of pro-inflammatory cytokines, but also potentially inhibits other processes that can augment the SAH associated inflammation. Further investigations are required to translate these findings in the clinical setting.
Subject: stroke
pattern recognition receptors
aneurysms
neuro-inflammation
post-SAH complications
1182 Biochemistry, cell and molecular biology
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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