CAJ | 학술논문

女性压力性尿失禁（ SUI）是一种常见病，但其发病机制目前尚无确切定论。近年来，试图通过研究SUI患者盆底支持组织中功能成分表达的病理性变化以探索SUI发病机制及相关治疗措施，已成为该领域的研究热点。该文综述了基质金属蛋白酶-3（MMP-3）、组织源性金属蛋白酶抑制剂-3（TIMP-3）、胶原（Collagen）Ⅲ、转化生长因子β1（TGF-β1）在SUI疾病发生、演化发展中的作用。
녀성압력성뇨실금（ SUI）시일충상견병，단기발병궤제목전상무학절정론。근년래，시도통과연구SUI환자분저지지조직중공능성분표체적병이성변화이탐색SUI발병궤제급상관치료조시，이성위해영역적연구열점。해문종술료기질금속단백매-3（MMP-3）、조직원성금속단백매억제제-3（TIMP-3）、효원（Collagen）Ⅲ、전화생장인자β1（TGF-β1）재SUI질병발생、연화발전중적작용。
Female stress urinary incontinence ( SUI) is a common disease , but its pathogenesis is currently not definite .In recent years , attempts by studying pathological changes of the functional components expressions in pelvic support tissues of SUI patients to explore SUI pathogenesis and relative therapeutic measures have become the hot point in this field . This paper reviewed the roles of matrix metalloproteinase-3(MMP-3), tissue inhibitor of metalloproteinase-3 (TIMP-3), collagenⅢ, transforming growth factor β1 (TGF-β1) in the occurrence , evolution and development of SUI .