Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review.
aneurysms
neuro-inflammation
pattern recognition receptors
post-SAH complications
stroke
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
18 Apr 2021
18 Apr 2021
Historique:
received:
23
03
2021
accepted:
12
04
2021
entrez:
30
4
2021
pubmed:
1
5
2021
medline:
25
5
2021
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 33919485
pii: ijms22084185
doi: 10.3390/ijms22084185
pmc: PMC8073517
pii:
doi:
Substances chimiques
Myeloid Differentiation Factor 88
0
Receptors, Pattern Recognition
0
Types de publication
Journal Article
Systematic Review
Langues
eng
Sous-ensembles de citation
IM
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