Abstract

RNA binding motif protein 15 (RBM15) has been implicated in the progression of various diseases. However, its role in intracerebral hemorrhage (ICH) remains inadequately understood. To investigate RBM15's involvement in ICH, an ICH model was established using HT-22 cells and C57BL/6 mice. Elevated RBM15 expression levels were observed, suggesting its critical role in ICH pathogenesis. Our study further revealed that RBM15 depletion significantly mitigated ICH-induced brain injury and enhanced neurological function. Furthermore, RBM15 was found to mediate the N6-methyladenosine (m6A) methylation of E2F transcription factor 1 (E2F1) mRNA, thereby enhancing its stability. Further analysis confirmed that RBM15 regulates mitophagy via E2F1, with E2F1 overexpression effectively counteracting mitophagy in the absence of RBM15. Collectively, these findings indicate that targeting RBM15 may offer a promising therapeutic strategy for ICH.