Rotator cuff injuries can be caused by a variety of factors, including degeneration, impingement, trauma, blood supply, fatty infiltration, etc. The incidence of rotator cuff injuries increases with age, mainly due to degeneration of tendon tissue. The special location of the rotator cuff results in a small soft tissue gap, which is prone to friction and impingement, resulting in edema, congestion, degeneration, and tearing of the rotator cuff. It has been found that the anterior 1/3 of the supraspinatus tendon, 1 cm from the stop of the supraspinatus, has a “lack of vascular zone”, and this weak zone is the center of tendon attachment. Once the contractile load of the supraspinatus muscle changes, it will spread to other weak areas and cause functional impairment. The large range of motion of the rotator cuff, the high oxygen consumption and the higher blood supply requirements will create a vicious circle and accelerate the disease progression. Changes in rotator cuff injury tendon tension directly affects the joint capsule tension and pressure direction, which activates the mechanical injury receptors around the joint, and the free nerve endings produce nociceptive impulses, which eventually act on the nociceptive center of the brain through afferent fibers. Both the stimulation of periarticular tension changes and the local tissue inflammatory response can trigger the release of a large number of endogenous nociceptive substances, leading to pain. Substance P, vascular endothelial growth factor, and the CXC family of chemokines mediate the pain mechanism of rotator cuff injury.