Genome-wide analysis of histone H3K18 lactylation in a kainic acid-induced epilepsy model

Metabolic reprogramming has been increasingly linked to epilepsy, but the epigenetic mechanisms connecting altered glucose metabolism to seizure susceptibility remain incompletely understood. In this study, we aimed to investigate whether lactate-associated histone modification contributes to epileptogenesis and to define its downstream transcriptional targets. Using a kainic acid (KA)-induced temporal lobe epilepsy model, we examined genome-wide chromatin occupancy of histone H3 lysine 18 lactylation (H3K18la) in control and epileptic mouse hippocampal tissues by ChIP-seq. The objective of this study was to characterize H3K18la-associated epigenetic changes during epileptogenesis and to identify candidate genes and pathways regulated by this histone mark. These data provide a genome-wide resource for understanding how glycolysis-related histone lactylation is involved in transcriptional regulation during seizure development.