Leni and Peter W. May Department of Orthopaedics, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Int J Exp Pathol. 2013 Aug;94(4):293-303. doi: 10.1111/iep.12031. Epub 2013 Jun 17.
Tendinopathies are common muskoloskeletal injuries that lead to pain and disability. Development and pathogenesis of tendinopathy is attributed to progressive pathological changes to the structure, function, and biology of tendon. The nature of this disease state, whether acquired by acute or chronic injury, is being actively investigated. Scarring, disorganized tissue, and loss of function characterize adult tendon healing. Recent work from animal models has begun to reveal the potential for adult mammalian tendon regeneration, the replacement of diseased with innate tissue. This review discusses what is known about musculoskeletal regeneration from a molecular perspective and how these findings can be applied to tendinopathy. Non-mammalian and mammalian models are discussed with emphasis on the potential of Murphy Roths Large mice to serve as a model of adult tendon regeneration. Comparison of regeneration in non-mammals, foetal mammals and adult mammals emphasizes distinctly different contributing factors to effective regeneration.
腱病是常见的肌肉骨骼损伤,可导致疼痛和残疾。腱病的发生和发病机制归因于肌腱结构、功能和生物学的进行性病理变化。这种疾病状态的性质,无论是急性还是慢性损伤引起的,都在被积极研究。疤痕、组织紊乱和功能丧失是成人肌腱愈合的特征。来自动物模型的最新研究开始揭示成年哺乳动物肌腱再生的潜力,即用固有组织替代患病组织。本文综述了从分子角度了解肌肉骨骼再生的情况,以及如何将这些发现应用于腱病。讨论了非哺乳动物和哺乳动物模型,并强调了 Murphy Roths Large 小鼠作为成人肌腱再生模型的潜力。非哺乳动物、胎生哺乳动物和成年哺乳动物的再生比较强调了有效再生的不同贡献因素。