ArticleImmunity, inflammation and disease2026
tRF-15:31-Arg-CCT-3-1 Improves Diabetic Kidney Disease by Reducing AATF and Alleviating Mesangial Cell Oxidative Stress and Inflammation.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- tRF-15:31-Arg-CCT-3-1 Improves Diabetic Kidney Disease by Reducing AATF and Alleviating Mesangial Cell Oxidative Stress and Inflammation.Immunity, inflammation and disease · 2026Article
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10 authors.
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Abstract
backgroundDiabetic kidney disease (DKD), a primary contributor to end-stage renal disease, involves a complex interplay between oxidative stress and inflammation. Given the reported involvement of apoptosis-antagonizing transcription factor (AATF) in cellular stress and inflammatory responses, we investigated whether the anti-inflammatory effects of tRF-15:31-Arg-CCT-3-1 (tRF-15:31) are mediated through the regulation of AATF expression.
methodsThe expression and biological effects of tRF-15:31 were investigated in streptozotocin (STZ)-induced DKD mice and high-glucose (HG)-treated renal mesangial cells. The involvement of AATF was examined through tRF-15:31 and AATF overexpression and siRNA-mediated knockdown of AATF.
resultsReduced expression of tRF-15:31 was observed in both STZ-induced DKD mice and HG-treated renal mesangial cells and was associated with aggravated intrarenal inflammation and oxidative stress. Overexpression of tRF-15:31 in diabetic mice significantly reduced serum creatinine levels and 24-h urinary protein excretion and alleviated renal pathological injury. Both in vivo and in vitro, tRF-15:31 overexpression markedly downregulated pro-inflammatory and oxidative stress markers, including IL-6, MCP-1, TNF-α, and malondialdehyde (MDA), while upregulating antioxidant factors such as glutathione (GSH) and glutathione peroxidase 4 (GPX4). AATF expression was significantly elevated in STZ-induced DKD mice, whereas this upregulation was markedly suppressed by tRF-15:31 overexpression. In HG-treated mesangial cells, co-overexpression of tRF-15:31 and AATF reversed the protective effects of tRF-15:31 overexpression alone. Furthermore, siRNA-mediated knockdown of AATF significantly attenuated HG-induced inflammation and oxidative stress.
conclusionCollectively, these findings suggest that tRF-15:31 attenuates inflammation and oxidative stress in the STZ-induced DKD model, at least in part through regulation of AATF expression. These findings provide additional mechanistic evidence for tRF-mediated regulation in DKD and support further investigation of the biological significance of the tRF-15:31-AATF regulatory relationship.
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