.png){kind=icon}
.png){kind=icon}
Return
Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration
.png){kind=icon}
PRE
AI
H
J
R
Z
K
DOI：10.1177/0271678x261468877.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
<jats:p>Subarachnoid hemorrhage (SAH) remains a leading cause of mortality and long-term disability worldwide. While the primary injury is defined by mechanical tissue disruption, the progression of secondary brain injury is largely driven by robust neuroinflammatory cascades initiated by blood derived damage-associated molecular patterns (DAMPs). Among the key mediators of this response, Toll-like receptor 4 (TLR4) has emerged as a central regulator. TLR4 activation in microglia triggers downstream signaling through both MyD88 and TRIF dependent pathways, driving the production of pro inflammatory cytokines and type I interferons. Additionally, non-canonical regulation of TLR4 by Lyn kinase introduces a critical modulatory mechanism that can shift microglial responses between inflammatory and phagocytic phenotypes in a sex dependent manner. Beyond hemorrhagic stroke, TLR4 mediated neuroinflammation also plays a significant role in the progression of Alzheimer’s disease, and other neurodegenerative disorders. Emerging therapeutic strategies targeting TLR4 and its downstream signaling components including small molecules, natural compounds, aptamers, and TLR4–Lyn interaction modulators demonstrate promising potential in attenuating neuroinflammation and improving neurological outcomes. This review highlights the molecular mechanisms of TLR4 signaling in neuroinflammation and underscores its translational relevance as a therapeutic target in both acute and chronic neurodegenerative conditions.</jats:p>
Journal
J
IF:
4.5
Papers:
5.9K
Citations:
2.1W
Organization
Cited Papers