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与正常妇女相比,子宫内膜异位症(EMs)妇女在位子宫内膜在基因表达上存在某些差异,已知有:巨噬细胞游走抑制因子(MIF)、血管内皮生长因子A(VEGF-A)、基质金属蛋白酶(MMP)、环氧合酶2(COX-2)和尿激酶型纤溶酶原激活物(uPA)过量表达,P450芳香化酶、c-kit异常或过量表达,17β羟类固醇脱氢酶(17β-HSD)、MMP组织抑制物(TIMP)和血浆素原活化因子抑制物(PAI)表达不足,雌激素和孕酮受体α/β比例异常。对孕酮反应性的改变可以解释MMP过量,MMP过量可以解释白细胞介素I的Ⅱ型受体(IL-1RⅡ)不足。在位内膜基因表达异常如果发生于EMs种植之前,则这类异常可能是EMs的原发病因环节。以上进展有助于解释EMs的病理过程,并可能为寻找新的诊断和治疗技术提供线索。
Women with endometriosis (EMs) have some differences in gene expression in the endometrium compared to normal women, known as macrophage migration inhibitory factor (MIF), vascular endothelial growth factor A (VEGF-A), matrix metalloproteinases (MMPs), cyclooxygenase 2 (COX-2) and urokinase plasminogen activator (uPA) overexpression, P450 aromatase, c-kit abnormalities or excess 17β-hydroxysteroid dehydrogenase (17β-HSD), tissue inhibitor of matrix metalloproteinase (TIMP) and plasma inhibitor of plasma actin (PAI) expression, estrogen and progesterone receptor α / β ratio is abnormal. Changes in reactivity to progesterone explain the excess of MMP, which may account for the lack of IL-1 receptor type II (IL-IRII). Eutopic endometrial gene abnormalities may occur as the primary cause of EMs if they occur prior to EMs implantation. These advances help explain the pathological process of EMs and may provide clues for finding new diagnostic and therapeutic techniques.