Deciphering the Role of N-Acetyltransferase 10 in Thalamic Hemorrhage Through Integrative Multi-Omics and Experimental Validation

Thalamic hemorrhage (TH) is a severe neurological condition, the molecular mechanisms of which are poorly understood, particularly in clinical settings. N-acetyltransferase 10 (NAT10), a regulator of RNA N4-acetylcytidine (ac4C) modification, has been implicated in cell cycle regulation and identified as a potential therapeutic target. This study explored the effects of NAT10 inhibition on TH pathology using a multi-omics approach. A mouse model of TH was established via collagenase IV injection. NAT10 activity was detected by dot blot and inhibited using Remodelin. Comprehensive multi-omics analyses, including 16S ribosomal Deoxyribonucleic Acid (16S rDNA) sequencing, metabolomics, and transcriptomics, were used. Behavioral, histological, and molecular evaluations were conducted to evaluate the key genes.