In the present study, we found that 1) DICAR overexpression inhibits brain impairment induced by stroke; 2) DICAR regulates the miR-361-3p/PRMT1 signaling pathway, thereby influencing angiogenesis in brain ECs; and 3) AAV9-DICAR-JP plays an important role in vascular remodeling following brain impairment. This evidence concerns the gene PRMT1 and Stroke.