Endometriosis is a complex disease with a multifactorial pathogenesis, which is crucially dependent on the neovascularization. The present review highlights the fact that the neovascularization of endometriotic lesions is not only driven by angiogenesis, but also involves de novo formation of microvessels from circulating endothelial progenitor cells (EPC). This process, termed vasculogenesis, is a characteristic of various pathogenic conditions, such as tumour growth and atherosclerosis, and typically comprises the activation, mobilization and recruitment of bone marrow-derived EPC to the sites of tissue hypoxia. Recent studies indicate that part of the microvascular endothelium of ectopic endometrial tissue originates from EPC, and controlled by the stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor type 4 (CXCR4) axis. Accordingly, blockade of EPC recruitment effectively inhibits the formation of microvascular networks in developing endometriotic lesions, indicating that vasculogenesis represents an integral part of the pathogenesis of endometriosis. The involvement of vasculogenesis in endometriosis may offer the exciting opportunity for the future establishment of novel diagnostic and therapeutic strategies for this frequent gynecological disease.%子宫内膜异位症(endometriosis,EMs)是一种复杂的多病因妇科疾病,EMs的发生、发展依赖于血管新生(neovascularization).EMs的血管新生包括血管生成(angiogenesis)和血管形成(vasculogenesis).血管形成是由循环中的内皮祖细胞(endothelial progenitor cell,EPC)参与的,此过程包括骨髓来源的EPC活化、动员和向外周组织的募集.除EMs外,血管形成还是肿瘤、动脉硬化等多种疾病的特征性病理变化.研究表明部分EMs病灶微血管内皮细胞是由EPC分化而来的,基质细胞衍生因子1(SDF-1)/CXC趋化因子受体4(CXCR4)轴参与了外周组织对EPC募集的调控,阻断EPC募集能有效地抑制异位病灶微血管的形成.抑制异位内膜中EPC介导的血管形成有望成为EMs抗血管治疗新的切入点.
展开▼
