背景:肌腱是一种连接骨骼和肌肉的纤维组织, 主要功能是在运动时从肌肉向骨骼传导应力, 肌腱病是临床常见的疾病类型, 表现为肌腱炎症、退变和损伤.细胞自噬广泛参与许多疾病的发展.基于细胞自噬的研究方法为肌腱损伤的修复提供了新的思路.目的:综述细胞自噬的发生过程和调控机制, 分析细胞自噬参与肌腱病的病理机制, 为肌腱病的预防治疗提供参考.方法:应用计算机检索中国知网、万方数据库及PubMed数据库关于自噬与肌腱病的相关研究的文章, 中文检索词为"自噬、肌腱、成纤维细胞、肌腱病", 英文检索词为"autophagy, tendon, fibroblast, tendinopathy".进行系统的归纳总结和分析, 排除内容相关性差或重复文献, 最终得到54篇文献.结果与结论:自噬可以减轻氧化应激对人肌腱干细胞的损害;随着肌腱组织的细胞外基质降解程度的增加, 肌腱细胞由于过度的细胞自噬出现自噬性细胞死亡;前列腺素E2以剂量依赖的方式显著诱导成纤维细胞的死亡和自噬;肩袖损伤后的肌肉萎缩受自噬调控;雷帕霉素通过自噬的激活抑制肌腱损伤后的腱周纤维化.综合目前研究结果, 自噬在肌腱病中有重要作用, 自噬将会成为肌腱病新的研究热点, 更加详细地了解自噬过程及其在肌腱病中的作用, 有助于研究人员找到肌腱病的靶向自噬途径, 为干预和治疗肌腱病提供新的理论和方法支持.%BACKGROUND: Tendon is a fibrous tissue that connects bone and muscle. The main function is to conduct stress from the muscles to the bone during exercise. Tendinopathy is a commonly seen disease, characterized by tendon inflammation, degeneration and injury. Autophagy is widely involved in the development of many degenerative diseases. The research method based on autophagy provides a new idea for tendon repair. OBJECTIVE: To review the process and regulation mechanism of autophagy, and to analyze the pathological mechanism of autophagy involved in the tendinopathy so as to provide a reference for the prevention and treatment of tendinopathy. METHODS: The articles concerning autophagy and tendinopathy were retrieved by computer in CNKI, WanFang and PubMed databases. The keywords were "autophagy, tendon, fibroblast, tendinopathy" in English and Chinese, respectively. Finally, 54 articles were obtained through systematic induction and analysis after excluding the irrelevant and repetitive articles. RESULTS AND CONCLUSION: Autophagy can alleviate the damage to human tendon stem cells induced by oxidative stress. With the increase of the degree of extracellular matrix degradation in the tendon tissue, autophagic cell death occurs in the tendon cells due to excessive autophagy. Prostaglandin E2 significantly induces fibroblast death and autophagy in a dose-dependent manner. The muscle atrophy after the rotator cuff injury is regulated by autophagy. Rapamycin prevents peritendinous fibrosis through activation of autophagy. In conclusion, autophagy plays an important role in tendinopathy. Autophagy will become a new hotspot in tendinopathy. Further understanding of autophagy and its role in tendinopathy will contribute to finding a targeted autophagy pathway and provide new theoretical and methodological support for the intervention and treatment of tendinopathy.
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