Yen Chih-Feng, Huang S Joseph, Lee Chyi-Long, Wang Hsin-Shih, Liao Shuen-Kuei
1 Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, Kwei-Shan, Tao-Yuan, Taiwan.
2 Department of Obstetrics and Gynecology, Chang Gung University College of Medicine, Kwei-Shan, Tao-Yuan, Taiwan.
Reprod Sci. 2017 Oct;24(10):1346-1361. doi: 10.1177/1933719117691141. Epub 2017 Feb 9.
Adenomyosis, which manifests with focally or diffusely scattered endometrial tissue within the uterine myometrium, is an endometriosis-like disease with controversial pathogenesis and compromised reproductive outcomes. This review, including the in vitro and in vivo studies performed on human or mouse models, is aimed to summarize the specific molecular characteristics of endometrium in the biochemical microenvironments of uterine adenomyosis. Many studies attributed the endometrium as the main cause of pathogenesis, with evidence of differential genetic expression and/or epigenetic modulation as well as estrogen-induced epithelial-mesenchymal transition. However, some studies indicated that the myometrium could play a role in the development of disease, based on findings of smooth muscle metaplasia and/or fibroblast-to-myofibroblast transdifferentiation by the influence of local biochemical factors. To date, it remains unclear whether adenomyosis is a genetically determined or a microenvironmentally induced disorder or whether the dysregulation of local factors may elicit the alteration of genetic expression in the endometrium. Similarly, it is uncertain whether the endometrial characteristics would remain consistent or could change along with a woman's reproductive life. Further longitudinal studies of the epigenetic controls or system biology are needed to elucidate the pathogenesis. Discovery of effective conservative treatments to improve the reproductive outcomes of patients with adenomyosis is still warranted.
子宫腺肌病表现为子宫肌层内局灶性或弥漫性散在的子宫内膜组织，是一种发病机制存在争议且生殖结局受损的子宫内膜异位症样疾病。本综述包括对人类或小鼠模型进行的体外和体内研究，旨在总结子宫腺肌病生化微环境中子宫内膜的特定分子特征。许多研究将子宫内膜归因于发病机制的主要原因，有差异基因表达和/或表观遗传调控以及雌激素诱导的上皮-间质转化的证据。然而，一些研究表明，基于平滑肌化生和/或成纤维细胞向肌成纤维细胞转分化受局部生化因素影响的研究结果，肌层可能在疾病发展中起作用。迄今为止尚不清楚子宫腺肌病是一种由基因决定的疾病还是由微环境诱导的疾病，或者局部因素的失调是否可能引发子宫内膜基因表达的改变。同样，不确定子宫内膜特征是否会保持一致或是否会随着女性的生殖生命而改变。需要进一步进行表观遗传控制或系统生物学的纵向研究以阐明发病机制。发现有效的保守治疗方法以改善子宫腺肌病患者的生殖结局仍然是必要的。
