子宫内膜异位症（内异症）为育龄妇女常见病，严重影响患者的工作能力和生活质量，为当今严重影响公共卫生的疾病。尽管对内异症已有大量的研究，但其发病机制不明。我们最近发表的研究表明：在内异症病灶中聚集的血小板显著高于于正常内膜，且血小板和病灶细胞相互对话，促进病灶的发展。而由于周期性出血，内异症病灶可以看成是一个不断损伤、不断修复的伤口。我们前期的研究表明：作为这样的一个伤口，内异症病灶与其微环境、尤其是血小板、巨噬细胞、NK细胞及中性粒细胞相互影响、互相作用，促进内异症病灶的发生和发展。本项目着重研究血小板、雌激素、及巨噬细胞对内异症发生发展的影响及其机制，研究血小板介导的NK细胞杀伤力的降低机制，研究中性粒细胞在内异症病灶形成初期的作用及其机制，识别出基于炎症／凝血状态通路的、新的内异症生物标记物，并试图从微环境的角度阐明内异症发生发展的机制，为临床诊断和药物开发提供有价值的工具和思路。

Endometriosis is a fairly common disease in women of reproductive age, impacting negatively on their productivity and quality of life. It is now recognized as a disease of public health concern. Despite extensive research, little is known regarding the pathophysiology of endometriosis. Our recently published studies indicate that platelets aggregate in ectopic endometrium, and there are extensive cross-talks between platelets and endometriotic implants. As lesion experiencing cyclic bleeding, endometriotic lesions can be viewed as a wound that experience repeated injury and repair. Our preliminary data indicate that, as such, endometriotic lesions interact with their microenvironment, especially with platelets, macrophages, NK cells, and neutrophils, accelerating the progression of endometriosis. We propose to investigate the endometriotic lesions and their microenvironment, and their interactions. In particular, we propose to investigate the effect of platelets and macrophageson the development of endometriosis, in the presence of estrogen; the cause as why the cytotoxicity of NK cells is reduced in endometriosis, and the role of neutrophils in the genesis and the development of endometriosis. In addition, we propose to identify coagulation-based biomarkers for endometriosis. Through these investigations, we hope to shed new light on the pathophysiology of endometriosis, opening new avenuse for the development of new diagnostic and therapeutic tools.