Adenomyosis is a benign lesion caused by the invasion of the uterine base by the basal layer of the uterus, with clinical manifestations of progressive dysmenorrhea, excessive menstruation, infertility and uterine enlargement. The etiology of adenomyosis is unclear, and the possible factors are thought to be genetic, injury (e.g., curettage and cesarean section), hyperestrogenemia, and viral infection. The prevalence of adenomyosis is as high as 13.4%, and the dysmenorrhea it causes seriously affects the work and life of patients. The diagnosis of this disease used to be based on clinical symptoms and signs, laboratory indicators (serum CA125 level), ultrasonography, etc. Uterine adenomyosis is a benign tumor with proliferative and invasive growth characteristics, and like tumors, its survival and development depends on angiogenesis. In addition to providing nutrients to the ectopic endometrium and discharging metabolites, the large number of neovascularization also provides infiltration and metastasis channels. The neointimal endothelial cells can also release a large amount of pro-angiogenic factors, prompting the formation of more blood vessels, thus forming a vicious circle, providing conditions for the endometrium to invade the myometrium and further invade and develop, and the lesions keep expanding, thus promoting the occurrence and development of the disease. At present, the main clinical treatment for adenomyosis is surgery and medication. Surgery is the most common method for traditional treatment of adenomyosis, including hysterectomy, simple lesion removal, endometrial resection, etc. Hysterectomy can treat the disease more thoroughly and with fewer complications, but it is usually applied to patients without fertility requirements and with poor results of conservative treatment, and is not used for young women with fertility requirements; simple focal resection has more difficulties and is not easy to remove the lesions completely, and is prone to recurrence after surgery. Endometrial resection is currently effective for superficial lesions, but it is not effective in controlling bleeding in lesions with an infiltration depth of >2 mm. Drug treatment mainly includes gonadotropin-releasing hormone (GnRHa), levonorgestrel intrauterine delayed-release system, oral contraceptives, progestin, etc. GnRHa can significantly reduce the active phase of adenomyosis, but it cannot cure the disease, is prone to recurrence, is expensive, and its adverse effects limit its long-term application. Relevant studies have found that levonorgestrel intrauterine delayed-release system has achieved better results in the treatment of adenomyosis, but the method is only effective in the short term, and relapses quickly once the course of treatment is over. It can be seen that drug treatment is often ineffective in patients with severe disease and is prone to relapse, and inevitably brings some adverse effects, such as causing endocrine disorders, early onset of menopausal syndrome or osteoporosis. Uterine artery embolization is an emerging method for the treatment of adenomyosis at home and abroad in recent years, which is now mature and widely promoted. It has been proven to be significantly more effective than drug therapy, avoiding adverse drug reactions and the more invasive surgery, overcoming the loss of fertility and psychological burden caused by removal of the uterus. Under normal conditions, there is no submucosal layer between the basal layer of the endometrium and the myometrium, and the myometrium has the ability to defend against endometrial invasion. Under the stimulation of inflammation and high estrogen, the defensive ability of the myometrium is damaged and the basal layer of the endometrium invades directly into the myometrium; microscopic damage to the myometrium caused by trauma such as childbirth and abortion allows the endometrium of the basal layer of the uterus to invade the myometrium along the site of microscopic damage. The ectopic endometrium has the function of synthesizing estrogen, which increases the local estrogen level, further promoting the growth of ectopic endometrium and hypertrophy of the normal myometrium. All ectopic endometrium is located in the myometrium, and all of them are supplied by uterine arteries, which provides a vascular anatomical basis for interventional treatment; ectopic endometrium is mostly in the proliferative stage and is sensitive to ischemia and hypoxia, which provides a pathological basis for interventional treatment; the blood flow in ectopic endometrium is richer than that in normal myometrium, which provides an imaging basis for the assessment of efficacy and safety of interventional treatment. The blood supply to the ectopic endometrium originates only from the uterine artery and lacks vascular traffic branches. Embolization of the trunk and peripheral vessels of the uterine artery with tiny granular embolic substances results in complete devascularization, which causes ischemic degeneration, necrosis, resorption, and atrophy of the diseased tissue, improves clinical symptoms, preserves the uterus, and maintains its normal physiological function. Adenomyosis is hormone-dependent, and embolization blocks the blood supply to the lesion, thus preventing hormones from entering the focal structures via the bloodstream to form low estrogen levels, causing a microenvironment similar to menopause, causing further atrophy of the lesion, and achieving the goal of treating adenomyosis. The advantages of uterine artery embolization: 1, can avoid open surgery, blood transfusion, can retain the integrity of the uterus; 2, retain the physiological function of the uterus and ovaries, improve the quality of life of patients with adenomyosis; 3, in case of incomplete one-time treatment or recurrence of lesions, can be treated several times by the same route; 4, if the embolization is not effective, other methods of treatment can still be used; 5, good efficacy, fast results The treatment is effective and quick to recover, with short hospitalization time, especially for symptomatic adenomyosis.