Knockdown of S100A11 Inhibits H₂O₂-Induced Oxidative Stress and Cellular Damage in Human Tenocytes

抄録

Rotator cuff tears (RCTs) are a leading cause of shoulder pain and dysfunction, often linked to oxidative stress and chronic inflammation. However, the molecular mechanisms underlying these pathological processes are not yet fully understood. S100A11, a calcium-binding protein of the S100 family, has been implicated in various inflammatory and degenerative diseases, but its role in RCTs is still unclear. In this study, we investigated the function of S100A11 in hydrogen peroxide H₂O₂-induced oxidative and inflammatory injury in human tenocytes. Our results demonstrated that S100A11 expression was significantly upregulated in tendon tissues from RCT patients. Knockdown of S100A11 markedly inhibited H₂O₂-induced inflammatory responses by reducing iNOS and PGE₂ levels and improved tenocyte viability. Furthermore, silencing S100A11 alleviated oxidative stress. Mechanistically, S100A11 knockdown activated the PI3K/Akt signaling pathway, suggesting a protective regulatory role. These findings highlight S100A11 as a potential therapeutic target for mitigating oxidative damage and promoting tendon repair in rotator cuff injuries.