ArticleRenal failure2026
tRF-1-ArgTCG-1-1 promotes renal fibrosis by regulating β-catenin.
Article in Renal failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRenal fibrosis (RF) is a crucial pathological factor in the progression of chronic kidney disease (CKD) to end-stage renal failure. The role of noncoding RNAs (ncRNAs) in CKD has been researched recently. tRNA-derived fragments (tRFs) constitute a class of small ncRNAs originating from tRNAs. To date, the function of tRFs in RF remains unexplored.
methodsHuman small RNA microarray analysis was performed to identify dysregulated tRFs in urine-derived renal tubular epithelial cells from patients with RF. RT-PCR was used for validation in clinical samples. Hydroxylamine-mediated protein precipitation mass spectrometry (Hypro-MS), parallel reaction monitoring (PRM), and antisense oligonucleotide (ASO)-mediated knockdown were used to investigate the interaction between tRF-1-ArgTCG-1-1 and β-catenin and its functional role in TGF-β1-treated HK-2 cells.
resultsMicroarray profiling identified tRF-1-ArgTCG-1-1 as an upregulated tRF in urine-derived renal tubular epithelial cells from patients with RF. RT-PCR further confirmed that tRF-1-ArgTCG-1-1 expression was significantly increased in urine samples from patients with CKD and was associated with impaired renal function and a higher risk of RF. Hypro-MS and PRM analyses demonstrated an interaction between tRF-1-ArgTCG-1-1 and β-catenin. ASO-mediated silencing of tRF-1-ArgTCG-1-1 reduced β-catenin expression in HK-2 cells. Moreover, silencing of tRF-1-ArgTCG-1-1, alone or together with β-catenin, attenuated TGF-β1-induced expression of RF-related markers
conclusionsOverall, these findings suggest that renal tubular epithelial cells tRF-1-ArgTCG-1-1 play a key role in RF and that the tRF-1-ArgTCG-1-1/β-catenin pathway is a potential therapeutic target for CKD and RF.
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