Description: | To explore the role of tRFs in TIF during DN progression, the present study performed high-throughput sequencing to detect differential expression profiles of tRFs in high glucose (HG)-treated tubular epithelial cells. Bioinformatics analyses were then conducted on these differentially regulated tRFs (fold change >2, P<0.05). The potential effect of specific tRF was investigated on HG-induced ECM accumulation of tubular epithelial cells. Therefore, the present study attempted to reveal the underlying mechanism of TIF from the novel perspective of tRFs and provide a promising therapeutic target for DN. |