Benign prostatic hyperplasia (BPH) is one of the most common benign diseases causing urinary disturbances in middle-aged and older men. The main manifestations are histological enlargement of the interstitial and glandular components of the prostate, anatomical enlargement of the prostate, clinical symptoms dominated by lower urinary tract symptoms (LUTS), and urodynamic obstruction of the bladder outlet (BOO). The incidence of histologic BPH increases with age, usually occurring initially after age 40 years, to >50% by age 60 years, and up to 83% by age 80 years. Similar to the histologic presentation, symptoms such as dyspareunia increase with age. Approximately 50% of men with a histologic diagnosis of BPH have moderate to severe lower urinary tract symptoms. Some studies have shown that it appears that Asians are more likely to have moderate-to-severe BPH-related symptoms than Americans. Two important conditions must be present for BPH to occur: advancing age and a functioning testis. Domestic scholars investigated 26 elderly Qing dynasty eunuchs and found that 21 had completely inaccessible or significantly atrophied prostates. However, the specific mechanism by which BPH occurs is unclear and may be caused by a balanced disruption of epithelial and mesenchymal cell proliferation and apoptosis. Associated factors are: androgens and their interaction with estrogens, prostatic mesenchymal-adenoepithelial cell interactions, growth factors, inflammatory cells, neurotransmitters and genetic factors. Prostatic hyperplasia leads to prolongation, pressure deformation and narrowing of the posterior urethra and increased urethral resistance, resulting in a series of changes in bladder function and the upper urinary tract. Due to the increase in bladder pressure, compensatory hypertrophy of the bladder forcing muscle, instability of the forcing muscle and reduced bladder compliance occur; if the obstruction is not lifted for a long time, the forcing muscle loses its compensatory capacity. The thickening of the bladder forcing muscle can make the ureteral bladder wall segment lengthen and stiffen, resulting in mechanical obstruction of the ureter; after the bladder loses its compensatory capacity, the ureteral bladder wall segment can shorten again, and coupled with the increase in bladder pressure, ureteral reflux can occur, eventually leading to hydronephrosis and renal function impairment.