Ker Robert F
School of Biology, The University of Leeds, Leeds LS2 9JT, UK.
Comp Biochem Physiol A Mol Integr Physiol. 2002 Dec;133(4):987-1000. doi: 10.1016/s1095-6433(02)00171-x.
Different tendons are (i) subject to very different stresses from their muscles and (ii) differ in their susceptibility to fatigue damage. The fatigue quality of each tendon is matched to the stress it experiences, so that, in life, all tendons are similarly prone to damage. On-going damage must be routinely repaired to maintain homeostasis and prevent damage from becoming symptomatic. The discovery of major differences in fatigue quality among tendons, which had previously seemed fairly similar in their mechanical properties, raises a wide range of new questions. (A) What structural and chemical differences underlie the variations in fatigue quality? (B) What molecular structure in the tendon is damaged and how is repair organised? (C) Is fatigue quality adaptable and if so what is the trigger for adaptation? Putting these questions into context leads to an integrated review of tendon, including structure and chemistry, the turnover of proteins, the cross-linking of collagen and the response of tenocytes to load on the tendon.
不同的肌腱（i）承受来自其肌肉的应力差异很大，（ii）对疲劳损伤的易感性也不同。每条肌腱的疲劳特性都与其所承受的应力相匹配，因此在生命过程中，所有肌腱发生损伤的可能性相似。持续的损伤必须定期修复以维持体内平衡，并防止损伤出现症状。此前在力学性能上看似相当相似的肌腱，其疲劳特性却存在重大差异，这一发现引发了一系列新问题。（A）导致疲劳特性变化的结构和化学差异是什么？（B）肌腱中的何种分子结构受到损伤，修复是如何组织的？（C）疲劳特性是否具有适应性，如果是，适应性的触发因素是什么？将这些问题置于背景中进行考量，会促成对肌腱的综合综述，内容包括结构与化学、蛋白质更新、胶原蛋白交联以及肌腱细胞对肌腱负荷的反应。
