Shetye Snehal S, Tamburro Margaret K, Fung Ashley K, Leahy Thomas P, Magee Madison N, Raja Harina A, Weiss Stephanie N, Nuss Courtney A, Farber Daniel C, Soslowsky Louis J
McKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, University of Pennsylvania, Philadelphia, Pennsylvania, United States.
Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, United States.
Am J Physiol Cell Physiol. 2025 Jun 1;328(6):C2013-C2022. doi: 10.1152/ajpcell.00186.2025. Epub 2025 May 8.
Despite the high prevalence of Achilles tendinopathy, clinically relevant animal models of Achilles tendinopathy are lacking. Previous studies have demonstrated possible tendinopathic cell and matrix changes with high-speed treadmill running, but the consistency as well as functional and mechanical consequences of these changes were unclear. We sought to determine the applicability of this protocol as a tendinopathy model by defining changes in Achilles tendon structure, function, and mechanics associated with 16 wk of high-speed treadmill running (26.8 m/min, 60 min/day, and 5 days/wk). We expected that high-speed running would induce detrimental structural, functional, and mechanical changes that worsen over the course of the 16-wk protocol. Treadmill running did influence body weight, hindlimb gait, and tendon cross-sectional area. However, contrary to our hypothesis, treadmill running did not induce tendinopathic changes in matrix organization, cell morphology, or tendon mechanics. As such, alternative strategies for robust and reproducible induction of Achilles tendinopathy in preclinical animal models are needed. We demonstrated that 16 wk of high-speed treadmill running did not induce structural, functional, or mechanical changes consistent with Achilles tendinopathy in the rat. These findings underscore the importance of exploring alternative approaches to generating reliable and clinically relevant animal models of Achilles tendinopathy.
尽管跟腱病的患病率很高，但缺乏与临床相关的跟腱病动物模型。先前的研究表明，高速跑步机跑步可能会导致跟腱细胞和基质发生病变，但这些变化的一致性以及功能和力学后果尚不清楚。我们试图通过确定与16周高速跑步机跑步（26.8米/分钟，每天60分钟，每周5天）相关的跟腱结构、功能和力学变化，来确定该方案作为跟腱病模型的适用性。我们预计高速跑步会导致有害的结构、功能和力学变化，且在16周的实验过程中会逐渐恶化。跑步机跑步确实影响了体重、后肢步态和肌腱横截面积。然而，与我们的假设相反，跑步机跑步并未在基质组织、细胞形态或肌腱力学方面诱导出跟腱病变化。因此，需要在临床前动物模型中采用其他策略来可靠且可重复地诱导跟腱病。我们证明，16周的高速跑步机跑步并未在大鼠身上诱导出与跟腱病一致的结构、功能或力学变化。这些发现强调了探索替代方法以建立可靠且与临床相关的跟腱病动物模型的重要性。
