Objective: To explore the role and mechanism of tRNA-derived fragment-011690（tRF-011690）) in Adriamycin induced podocyte autophagy. Methods: (1) Podocytes were intervened with ADR (1 μg/mL) and tRF-011690 mimic, and were divided into Control group, ADR group, ADR+tRF-011690 mimic group and ADR+tRF-011690 NC group. The mRNA expression levels of tRF-011690, LC3II/Ⅰ and p62 were detected by RT-qPCR; Western blot was used to determine the expression of LC3II/Ⅰ and p62 protein. (2) Podocytes were intervened with ADR (1 μg/mL) and Rapamycin and divided into Control group, ADR group,ADR+Rapamycin group and Rapamycin group. The relative expression of p-mTOR, LC3II/Ⅰ and p62 proteins was detected by Western blot, and RT-qPCR was used to detect the expression level of tRF-011690. Results：(1) Compared with Control group, the expression level of tRF-011690 was decreased in ADR group, and the expression of LC3II/Ⅰ and p62 was significantly increased at protein and mRNA levels (P<0.05). Compared with ADR+NC group, tRF-011690 expression level in ADR+tRF-011690 mimic group increased significantly (P<0.05), which confirmed the tRF-011690 was successfully overexpressed, and LC3 II/Ⅰ and p62 expression decreased significantly under protein and mRNA levels P<0.05). (2) Compared with Control group, p-mTOR protein expression was increased in ADR group, relative expression of LC3 II/Ⅰ and p62 protein was decreased, and tRF-011690 expression level was decreased (P<0.05); compared with ADR group, p-mTOR protein expression was decreased in ADR+Rapamycin group, relative expression of LC3 II/Ⅰ and p62 protein was decreased and tRF-011690 expression significantly increased (P<0.05). Conclusion: tRF-011690 may act as a downstream effector molecule of the mTOR pathway, which provides a new approach for the treatment of chronic kidney disease.