Abstract：
Since the first description of adenomyosis more than 150 years ago, multiple hypotheses have attempted to explain its pathogenesis. Indeed, research over recent years has greatly enhanced our knowledge of the underlying causes. This has opened up avenues for the development of strategies for both disease prevention and treatment of its main symptoms, such as pelvic pain, heavy menstrual bleeding, and infertility. However, the current means are still largely ineffective, so it is vital that we shed light on the pathways involved. Dysregulated mechanisms and aberrant protein expression have been identified as contributing factors in interactions between endometrial epithelial and stromal cells, ultimately leading to the growth of adenomyotic lesions. These include collective cell migration, epithelial-to-mesenchymal transition, hormonal influence, and signaling from non-coding RNAs and extracellular vesicles. We provide a concise summary of the latest insights into the crosstalk between glands and stroma in ectopic adenomyotic lesion formation. While there is an abundance of literature on similarities between adenomyosis and deep endometriosis, there are insufficient data on the cytochemical, molecular, and pathogenetic mechanisms of these two disorders. However, various shared features, including alterations of cell adhesion molecules, abnormal hormone regulation, and the presence of cancer-driving mutations and epigenetic modifications, have been identified. Nevertheless, the pathogenic mechanisms that contribute to the cause and development of these enigmatic diseases have not been fully elucidated yet.
摘要：
自从150多年前首次描述子宫腺肌病以来，多种假说试图解释其发病机制。的确,近年来的研究大大提高了我们对根本原因的认识。这为制定疾病预防和治疗其主要症状的策略开辟了途径，如骨盆疼痛，大量月经出血,和不孕症。然而,目前的手段仍然基本上无效，因此，我们必须阐明所涉及的途径。失调的机制和异常蛋白表达已被确定为子宫内膜上皮细胞和基质细胞之间相互作用的促成因素。最终导致腺病毒病变的生长。这些包括集体细胞迁移，上皮-间质转化，荷尔蒙的影响，以及来自非编码RNA和细胞外囊泡的信号传导。我们提供了有关异位腺体病变形成中腺体与基质之间串扰的最新见解的简要摘要。虽然有大量的文献关于子宫腺肌病和深子宫内膜异位症之间的相似性，关于细胞化学的数据不足，分子，以及这两种疾病的发病机制。然而,各种共享功能，包括细胞粘附分子的改变，激素调节异常,以及癌症驱动突变和表观遗传修饰的存在，已被确认。然而，导致这些神秘疾病的病因和发展的致病机制尚未完全阐明。
