TGF-β1与腱病关系的研究进展

Progress on relationship between transforming growth factor-beta1 and tendinopathy

腱病是常见的软组织疾病,但其发病机制尚未阐明并缺乏有效治疗手段。组织纤维化改变是其最主要的病理学特点之一。转化生长因子β1(transforming growth factor-beta1,TGF-β1)是参与纤维化的重要因子,它在腱病组织中的表达并不一致,仍存在争议。但绝大多数研究显示TGF-β1有异常表达,且以升高为主,表明TGF-β1在腱病发病过程中起重要作用。在肌腱的损伤和修复过程中,TGF-β1增高的时间点并不一致,其在肌腱修复中发挥作用的时间目前尚无定论。因TGF-β1在肌腱腱病和肌腱修复这两个看似相反的过程中都有异常表达,所以推测它并非一种单向调节的因子,而是具有多效性的。目前研究认为TGF-β1的作用途径是TGF-β1与受体相结合,将信号传入细胞,现在发现其受体有3种。TGF-β1在细胞内信号传导的经典通路主要是通过激活Smad通路进行的,同时也存在一些非经典通路。TGF-β1可以打破细胞外基质的平衡,这可能是造成腱病的一个途径,但其对细胞外基质的调控是复杂且多样的,需要深入研究。现有研究显示,阻断TGF-β1的下游通路对改善腱病的作用不佳,因此可以尝试对TGF-β1产生的上游机制进行研究,从寻找TGF-β1产生源头出发,或许可以找到更好的抑制腱病发生发展的新靶点。

As a common soft tissue disease,the mechanism of tendinopathy has not been clarified and is lack of effective treatment method.Change of tissue fibrosis is the one of the main pathological features.Transforming growth factor beta 1(TGF-β1),which is one of the important factor,participated in fibrosis.Inconsonant expressions of TGF-β1 could be found in tendinopathy.The studies are still controversial,but the vast majority of studies had showed that TGF-β1 was abnormal,and it is given priority to increase,which means that TGF-β1 plays an important role in the process of tendinopathy.In the process of tendon injuries and repairs,the time of TGF-β1 increasing is inconsistent.The time for TGF-β1 plays a significant role has not been determined.TGF-β1 has abnormal expressions in both tendinopathy and tendon repairs,which are two opposite processes.Thus,it may not be a one-way adjustment factor,but has a pleiotropic.Recent studies showed that TGF-β1 was considered as binding to receptor and transferring signal into the cell.Now there are three different receptors are found.The classical pathway of TGF-β1 in intracellular signal transduction is mainly through activation of Smad pathway.In the same time,there are also some non-classical pathways.TGF-β1 could break balance of extracellular matrix,which may be a reason to cause tendinopathy.But the regulations of TGF-β1 on the extracellular matrix are complex and diverse,further studies are required.Existing researches showed that the performance of treatments on tendinopathy is unsatisfied by blocking TGF-β1 downstream pathway.Therefore,it is a good way to studythe upstream mechanism of produce TGF-β1.It may be an effective method to find new targets to inhibit the development of tendinopathy better by finding the original source of TGF-β1.