Erratum: Autophagy Prevents Oxidative Stress-Induced Loss of Self-Renewal Capacity and Stemness in Human Tendon Stem Cells by Reducing ROS Accumulation

<b><i>Background/Aims:</i></b> Tendon stem cells (TSCs) exhibit a high self-renewal capacity, multi-differentiation potential, and low immunogenicity; thus, these cells might provide a new cell source for tendon repair and regeneration. TSCs are exposed to increased oxidative stress at tendon injury sites; however, how TSCs maintain their stemness under oxidative stress is not clear. Methods and <b><i>Results: </i></b>In this study, we found that H<sub>2</sub>O<sub>2</sub> treatment increased ROS accumulation in human TSCs (hTSCs) and resulted in loss of self-renewal capacity and stemness, as reflected in reduced colony formation and proliferation, decreased expression of the stemness markers Nanog, Oct-4, NS, and SSEA-4, and impaired differentiation capability. These H<sub>2</sub>O<sub>2</sub>-induced damages were prevented by pretreatment with starvation or rapamycin. Pretreatment with starvation or rapamycin prior to H<sub>2</sub>O<sub>2</sub> exposure also led to decreased intracellular and mitochondrial ROS accumulation along with increased autophagic activity, as manifested in increased LC3 cleavage, Beclin-1 expression, and GFP-LC3-labeled autophagosome formation. Autophagy inhibition by 3-MA or CQ, or by shRNA silencing of Agt-7 or Beclin-1 reduced the protective effects of starvation and rapamycin on H<sub>2</sub>O<sub>2</sub>-treated hTSCs. <b><i>Conclusion:</i></b> Thus, the findings of this study suggest that autophagy prevents oxidative stress-induced loss of self-renewal capacity and stemness in hTSCs through suppression of ROS accumulation.