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.

BACKGROUND Convulsive status epilepticus (CSE) triggers profound neuroinflammatory responses that exacerbate neuronal injury and impair long-term neurological recovery. FKBP5, a co-chaperone protein implicated in immune regulation, has been increasingly recognized as a modulator of inflammatory signaling. However, its...

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