Abstract: Endometriosis is a common gynecological disease characterized by the persistence and growth of vascularized endometrial tissue at ectopic sites, whose mechanisms are still poorly understood. Recently, studies have suggested that macrophages, which are the most abundant cells in the peritoneal fluid, play a critical role in the pathogenesis and pathophysiology of endometriosis. Macrophages are recruited to the microenvironment of endometriosis and infiltrate endometriotic lesions where they undergo alternative activation. These macrophages secrete various cytokines that stimulate adhere, growth, invasion and deliver signals. Macrophages facilitate endometrial cell survival mainly because of their impaired phagocytosis and increased apoptosis, thus create an immune tolerant environment. Microphages produce VEGF and express Tie-2 to promote angiogenesis and enhance endometrial lesions growth. The endometriosis-promoting functions of macrophages is associated with their "alternatively activated" phenotype involved in tissue repair and remodel. This review focuses on the roles and functions of macrophages in endometriosis. And further study revealing molecular mechanisms of macrophages would encourage the development of novel diagnosis and treatments for endometriosis.