The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.

肌腱干/祖细胞（TSPC）衰老与肌腱衰老之间的联系已得到公认。但是，TSPCs衰老的细胞和分子机制仍不完全清楚。在本研究中，我们调查了水通道蛋白1（AQP1）在TSPC衰老中的作用。我们显示，AQP1表达在肌腱老化过程中随年龄下降。在衰老的TSPC中，AQP1的过表达显着减弱了TSPC的衰老。另外，AQP1的过表达也恢复了与年龄有关的自我更新，迁移和肌腱分化的功能障碍。此外，我们证明了JAK-STAT信号传导通路在衰老的TSPC中被激活，AQP1的过表达抑制了JAK-STAT信号通路的激活，这表明AQP1通过抑制JAK-STAT信号通路减弱了TSPC的衰老和与年龄有关的功能障碍。综上所述，我们的发现证明了AQP1在调节TSPC衰老中的关键作用，并为拮抗肌腱衰老提供了新的靶点。