摘要
子宫腺肌病是一种常见的良性妇科疾病,表现为在位子宫内膜腺体和间质侵入到子宫肌层,使子宫弥漫性增大。子宫腺肌病虽是良性病变,但同时具有恶性肿瘤的一些生物学特征,如无限制生长、生成新血管和减少凋亡细胞数量等,其发病机制尚未明确。从自噬与细胞凋亡着手进行该病发病机制的研究已成热点。Beclin 1是调控自噬的重要基因,多种肿瘤存在Beclin 1自噬基因的缺陷;B细胞淋巴瘤/白血病2(Bcl-2)基因是一种原癌基因,其表达可抑制细胞凋亡。多项研究表明,在子宫腺肌病中,Beclin 1表达水平显著降低,Bcl-2表达水平显著升高,细胞自噬与凋亡功能缺失,两者共同作用导致子宫腺肌病发病。
Adenomyosis is a common benign gynecological disease characterized by endometrial glands and stromal cells invasion into the myometrium causing diffuse enlargement of uterus. Although adenomyosis is a benign disease, it has similar biological characteristics of malignant tumors, such as unlimited growth, generating new blood vessels and reducing the number of apoptotic cells. Its pathogenesis is not yet clear. Autophagy and apoptosis have become hot spots in the field. Beclin 1 is an important autophagy related gene, and many tumors present Beclin 1 gene defect. B cell lymphoma/leukemia 2 (Bcl-2) is a proto-oncogene, and its expression can inhibit cell apoptosis. Studies have shown that the expression of Beclin 1 is significantly lower and the Bcl-2 is evidently upregulated in adenomyosis. The disequilibrium of cell autophagy and apoptosis leads to the onset of adenomyosis.
出处
《医学综述》
2017年第24期4807-4811,共5页
Medical Recapitulate
基金
浙江省自然科学基金(LY15H040007)
作者简介
通信作者E-mail:zhengwei@zju.edu.cn