Targeting TLR4-dependent inflammation in post-hemorrhagic brain injury.

ABSTRACT: Recent data have implicated inflammation of the cerebrospinal fluid spaces after subarachnoid, intraventricular, and intracerebral hemorrhage to be a critical driver of multiple secondary brain injuries such as hydrocephalus, cerebral edema, and vasospasm. While TLR4-dependent reparative inflammation is an important protective response that can eliminate physical irritants and damaged cells, sustained or inappropriately triggered inflammation can initiate or propagate disease.Areas covered: We review recent advances in our understanding of how TLR4, including its upstream damage-associated molecular patterns and its downstream MyD88-dependent and independent signaling pathways, contributes to hemorrhage-induced inflammation in numerous brain diseases. We discuss prospects for the ph

SUBMITTER: Karimy JK 

PROVIDER: S-EPMC8104018 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature