Liver sinusoidal endothelial cells (LSECs) are key regulators of hepatic vascular homeostasis, and their capillarization accelerates liver fibrosis. While metastasis-associated protein 1 (MTA1) modulates angiogenesis, its role in LSECs during liver fibrogenesis remains unknown. In this study, we investigated the effect of endothelial-specific MTA1 deletion on LSEC phenotype and fibrotic progression using Tie2-Cre;Mta1^fl/fl mice in a CCl₄-induced liver fibrosis model.  Endothelial MTA1 deletion yielded striking sex-dimorphic phenotypes. In females, MTA1 deletion exacerbated liver injury and fibrosis, enhancing capillarization, as evidenced by elevated CD31 and reduced LYVE1 expression on liver immunofluorescence, accompanied by upregulated fibrogenic markers. Conversely, male knockouts displayed attenuated fibrosis with preserved LYVE1 and reduced CD31 expression. These divergent outcomes aligned with estrogen receptor alpha (ERα) expression, which decreased in female knockouts but increased in males. Ex vivo analysis of primary LSECs corroborated these findings, showing downregulation of endothelial function markers in females and upregulation in males. Collectively, our data establish that endothelial MTA1 differentially regulates LSEC capillarization and fibrotic progression in a sex-specific manner via ERα-associated signaling. These results identify MTA1 as a critical determinant of sex-divergent endothelial responses during liver fibrogenesis.