Wang Yifan, Dragovic Rebecca A, Greaves Erin, Becker Christian M, Southcombe Jennifer H
Nuffield Department of Women's and Reproductive Health, Oxford Endometriosis CaRe Centre, Nuffield University of Oxford, Oxford, United Kingdom.
Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry, United Kingdom.
Front Reprod Health. 2023 Apr 3;5:1130849. doi: 10.3389/frph.2023.1130849. eCollection 2023.
Endometriosis is an inflammatory disease that is defined as the growth of endometrium-like tissue outside the uterus, commonly on the lining of the pelvic cavity, visceral organs and in the ovaries. It affects around 190 million women of reproductive age worldwide and is associated with chronic pelvic pain and infertility, which greatly impairs health-related life quality. The symptoms of the disease are variable, this combined with a lack of diagnostic biomarkers and necessity of surgical visualisation to confirm disease, the prognosis can take an average timespan of 6-8 years. Accurate non-invasive diagnostic tests and the identification of effective therapeutic targets are essential for disease management. To achieve this, one of the priorities is to define the underlying pathophysiological mechanisms that contribute to endometriosis. Recently, immune dysregulation in the peritoneal cavity has been linked to endometriosis progression. Macrophages account for over 50% of immune cells in the peritoneal fluid and are critical for lesion growth, angiogenesis, innervation and immune regulation. Apart from the secretion of soluble factors like cytokines and chemokines, macrophages can communicate with other cells and prime disease microenvironments, such as the tumour microenvironment, the secretion of small extracellular vesicles (sEVs). The sEV-mediated intracellular communication pathways between macrophages and other cells within the peritoneal microenvironment in endometriosis remain unclear. Here, we give an overview of peritoneal macrophage (pM) phenotypes in endometriosis and discuss the role of sEVs in the intracellular communication within disease microenvironments and the impact they may have on endometriosis progression.
子宫内膜异位症是一种炎症性疾病，定义为子宫内膜样组织在子宫外生长，常见于盆腔腔内膜、内脏器官和卵巢。它影响着全球约1.9亿育龄妇女，与慢性盆腔疼痛和不孕有关，这极大地损害了与健康相关的生活质量。该疾病的症状多种多样，再加上缺乏诊断生物标志物以及需要手术可视化来确诊疾病，其预后平均需要6至8年时间。准确的非侵入性诊断测试和有效治疗靶点的识别对于疾病管理至关重要。要实现这一点，首要任务之一是确定导致子宫内膜异位症的潜在病理生理机制。最近，腹腔内的免疫失调与子宫内膜异位症的进展有关。巨噬细胞占腹腔液中免疫细胞的50%以上，对病变生长、血管生成、神经支配和免疫调节至关重要。除了分泌细胞因子和趋化因子等可溶性因子外，巨噬细胞还可以与其他细胞通信并塑造疾病微环境，如肿瘤微环境，通过分泌小细胞外囊泡（sEVs）。子宫内膜异位症中巨噬细胞与腹腔微环境中其他细胞之间的sEV介导的细胞内通信途径仍不清楚。在这里，我们概述了子宫内膜异位症中腹腔巨噬细胞（pM）的表型，并讨论了sEVs在疾病微环境内细胞内通信中的作用以及它们可能对子宫内膜异位症进展产生的影响。
