Department of Orthopaedics & Rehabilitation, Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
Connect Tissue Res. 2023 Jan;64(1):1-13. doi: 10.1080/03008207.2022.2102004. Epub 2022 Jul 28.
Aging is a complex and progressive process where the tissues of the body demonstrate a decreased ability to maintain homeostasis. During aging, there are substantial cellular and molecular changes, with a subsequent increase in susceptibility to pathological degeneration of normal tissue function. In tendon, aging results in well characterized alterations in extracellular matrix (ECM) structure and composition. In addition, the cellular environment of aged tendons is altered, including a marked decrease in cell density and metabolic activity, as well as an increase in cellular senescence. Collectively, these degenerative changes make aging a key risk factor for the development of tendinopathies and can increase the frequency of tendon injuries. However, inconsistencies in the extent of age-related degenerative impairments in tendons have been reported, likely due to differences in how "old" and "young" age-groups have been defined, differences between anatomically distinct tendons, and differences between animal models that have been utilized to study the impact of aging on tendon homeostasis. In this review, we address these issues by summarizing data by well-defined age categories (young adults, middle-aged, and aged) and from anatomically distinct tendon types. We then summarize in detail how aging affects tendon mechanics, structure, composition, and the cellular environment based on current data and underscore what is currently not known. Finally, we discuss gaps in the current understanding of tendon aging and propose key avenues for future research that can shed light on the specific mechanisms of tendon pathogenesis due to aging.
衰老是一个复杂且渐进的过程，在此过程中，身体组织表现出维持内稳态的能力下降。衰老时，会发生大量的细胞和分子变化，随后正常组织功能的病理性退变易感性增加。在肌腱中，衰老导致细胞外基质（ECM）结构和组成发生明显改变。此外，老化肌腱的细胞环境也发生了改变，包括细胞密度和代谢活性显著降低，以及细胞衰老增加。这些退行性变化共同使衰老成为发生腱病的关键风险因素，并增加肌腱损伤的频率。然而，已有研究报告称，肌腱中与年龄相关的退行性损伤的程度存在不一致性，这可能是由于“年轻”和“年老”年龄组的定义方式不同、解剖上不同的肌腱之间存在差异以及用于研究衰老对肌腱内稳态影响的动物模型之间存在差异所致。在这篇综述中，我们通过总结明确年龄类别（年轻人、中年人、老年人）和解剖上不同的肌腱类型的数据来解决这些问题。然后，我们根据现有数据详细总结了衰老如何影响肌腱力学、结构、组成和细胞环境，并强调了目前尚不清楚的内容。最后，我们讨论了当前对肌腱衰老理解的差距，并提出了未来研究的关键途径，这些研究可以阐明由于衰老导致的肌腱发病机制的具体机制。
