Microglial TLR7 contributes to traumatic brain injury-induced neuroinflammation in mice.

LncRNA UCA1 Aggravated Microglia-mediated Neuroinflammation After Traumatic Brain Injury by Targeting miR-708-5p

Intranasal CRISPR lipid nanoparticles targeting MAPK9 attenuate neuroinflammation after traumatic brain injury

It is demonstrated that intranasal delivery of Iba-1-targeted CRISPR-LNPs enables effective MAPK9 modulation in Iba-1 + myeloid cells within the injured brain and attenuates acute neuroinflammation following TBI.

Sult2b1 Modulates NLRP3/BCL-2 Signaling and Pro-Inflammatory Microglial/Macrophage Polarization After Traumatic Brain Injury.

The findings identify Sult2b1 as an endogenous protective factor that limits neuroinflammation and promotes neuronal survival via NLRP3/BCL-2 and microglial polarization modulation, suggesting therapeutic potential.

Microglial RIOK3 promotes post-ischemic neuroinflammation by facilitating YBX1 phosphorylation and nuclear accumulation.

Microglia-targeted RIOK3 knockdown reduced infarct volume, improved early neurological and sensorimotor outcomes, preserved microglial process complexity, and reduced post-ischemic inflammation, and highlight the RIOK-YBX1 axis as a potential therapeutic target for ischemic stroke.

FKBP5 promotes pro-inflammatory microglial activation and neuronal injury through NF-κB/NLRP3 signaling in convulsive status epilepticus.

This study identifies FKBP5 as an upstream modulator of NF-κB/NLRP3 signaling in microglia during convulsive status epilepticus and suggests targeting FKBP5 may represent a promising strategy to ameliorate neuroinflammation and neuronal injury in epilepsy.

ELAVL3 Exacerbates Brain Injury and Cognitive Dysfunction in Mice After Cardiac Arrest by Increasing S100B mRNA Stability to Promote Microglia Activation

This study identifies the ELAVL3/S100B axis as a key driver of post-ischemic neuroinflammation and Targeting this pathway may offer a potential therapeutic strategy for cerebral ischemic injuries.