Longo Umile Giuseppe, Oliva Francesco, Denaro Vincenzo, Maffulli Nicola
Department of Orthopaedic and Trauma Surgery, Campus Biomedico University, Via Longoni, Rome, Italy.
Disabil Rehabil. 2008;30(20-22):1563-71. doi: 10.1080/09638280701785643.
To review the current concepts on tendon damage and reactive oxygen species (ROS). We suggest that tendons are subject to reactive oxygen generated both within the vicinity of the tendon and from the tenocytes themselves.
A literature search was conducted to trace relevant literature on tendon damage and ROS.
Tendinopathies have a complex aetiology. Tendon physiology and structure may preclude ROS involvement in various aspects of the predisposition to and participation in a failed healing response process and subsequent response to injury. However, given the ubiquitous nature of ROS production and their now accepted involvement in signal transduction, such highly active chemicals may influence signal transduction in the tendon. Therefore, the tendon is continually exposed to ROS during normal and athletic exercise which, in combination with lifestyle and possibly hereditary factors, may influence tendon integrity and orchestrate tendon repair.
The production of ROS by tenocytes may be a response to hyperthermia and to repetitive ischaemia/reperfusion, and may influence the development of tendinopathies.
回顾当前关于肌腱损伤和活性氧（ROS）的概念。我们认为，肌腱会受到在肌腱附近以及由肌腱细胞自身产生的活性氧的影响。
进行文献检索以追踪有关肌腱损伤和ROS的相关文献。
肌腱病的病因复杂。肌腱的生理和结构可能使ROS无法参与到易感性的各个方面以及参与愈合反应失败过程和随后对损伤的反应。然而，鉴于ROS产生的普遍性以及它们目前被公认参与信号转导，这种高活性化学物质可能会影响肌腱中的信号转导。因此，在正常运动和体育锻炼期间，肌腱持续暴露于ROS中，这与生活方式以及可能的遗传因素相结合，可能会影响肌腱的完整性并协调肌腱修复。
肌腱细胞产生ROS可能是对高温和重复性缺血/再灌注的反应，并可能影响肌腱病的发展。
