March 3, 2026Open Access

Inhibiting H3K18 lactylation in microglia aggravates white matter injury after intracerebral hemorrhage in mice

Key Points

White matter injury is worsened by inhibiting h3k18 lactylation in microglia after intracerebral hemorrhage, indicating its protective role.
The critical protective axis involves lactate, p300/CBP, and h3k18 lactylation, highlighting an achievable neuroprotective strategy.
Assessment utilizing epigenetic markers and microglial activity underscores the intricate cellular mechanisms at play in brain repair.
Targeting this h3k18 lactylation pathway may enhance recovery post-intracerebral hemorrhage, but further studies are necessary.

Abstract

These results demonstrated that lactate-derived H3K18 lactylation (H3K18la), orchestrated by p300/CBP-mediated epigenetic reprogramming, serves as a critical endogenous neuroprotective axis of WMI following ICH. Microglia emerge as the cellular executors of this pathway. This lactate-p300/CBP-H3K18la axis thus represents a therapeutically targetable mechanism for enhancing post-hemorrhagic brain repair through microglia-guided myelin regeneration.

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Cite This Study

Jiang et al. (Wed,) studied this question.

synapsesocial.com/papers/69a75cbac6e9836116a25dd7 https://doi.org/https://doi.org/10.1016/j.brainresbull.2026.111744

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