Background The etiology of stress urinary incontinence (SUI) is complex and diverse among women, with past studies having demonstrated that estrogen de ciency is an important cause of pelvic oor muscle atrophy and urethral degeneration. We comprehensively investigated the effects of estrogen in the treatment of SUI in female mice at cellular and animal levels.Methods L929 cell mechanical injury model was established by four point bending device, and SUI mouse model was established by vaginal dilation method commonly used to simulate labor injury. After treatment, the expressions of collagen I, collagen III, elastin, TIMP-1, TIMP-2, MMP-2 and MMP-9 were detected, the leak point pressure (LPP) and abdominal leak point pressure (ALPP) of mice in each group were detected, and the effect of estrogen on extracellular matrix remodeling of mouse urethra and anterior vaginal wall was observed from the histological level.Results These results revealed that an appropriate amount of estrogen can promote the expression of collagen I, collagen III, elastin, TIMP-1, and TIMP-2, decrease the expression of MMP-2 and MMP-9, and maintain the dynamic balance of MMPs/TIMPs at both cellular and animal levels. Meanwhile, we determined that estrogen can increase the LPP and ALPP values of SUI mice. The collagen bers' content in the mice treated with estrogen was signi cantly greater than in the control group mice.Conclusions The estrogen may alleviate the symptoms of SUI by reconstituting ECM, toward laying a solid foundation for the further exploration of estrogen therapy.