子宫内膜异位症纤维化相关细胞及其活化机制研究进展  

Research progress of fibrosis-related cells and their activation mechanism in endometriosis

作　　者：王安琪 孙佳凡 徐炜[1] 王秀丽[1] WANG Anqi;SUN Jiafan;XU Wei;WANG Xiuli(Department of Gynecology,the First Affiliated Hospital of Nanjing Medical University,Nanjing 210029,China)

机构地区：[1]南京医科大学第一附属医院妇科,江苏南京210029

出　　处：《南京医科大学学报（自然科学版）》2022年第11期1637-1642,共6页Journal of Nanjing Medical University(Natural Sciences)

基　　金：江苏省妇幼健康重点人才课题(RC201709);江苏省卫生计生委科研课题(H2018017)。

摘　　要：子宫内膜异位症(endometriosis,EMS)近年来被认为是一种纤维化疾病,EMS病灶的纤维化与EMS相关的疼痛、不孕和药物耐药密切相关。肌成纤维细胞(myofibroblast,MFB)是EMS纤维化的关键细胞,MFB在EMS病灶中的来源多样,活化途径也有多种,抑制MFB活化、促进其凋亡或衰老可抑制组织纤维化。本文就EMS病灶纤维化与临床表现之间的相关性、异位内膜中MFB的来源和活化途径、靶向MFB抑制纤维化的研究进展进行综述。Endometriosis(EMS)has been recognized as a fibrotic disease in recent years,and the fibrosis process of EMS lesions is strongly associated with EMS-related pain,infertility and drug resistance. Myofibroblast(MFB)is the key cell of EMS fibrosis,MFB has a variety of cell sources in eutopic lesions and many activation pathways. Inhibiting MFB activation,promoting apoptosis or cell senescence can inhibit tissue fibrosis. In this paper,the research progress about the correlation between fibrosis and clinical manifestations of EMS,the sources and activation pathways of MFB in EMS,and targeting MFB to inhibit fibrosis are reviewed.

关 键 词：子宫内膜异位症 肌成纤维细胞 纤维化 转化生长因子-Β 

分 类 号：R711.71[医药卫生—妇产科学]