tRFs在足细胞损伤与凋亡机制中的研究进展：以阿霉素肾病为模型的新视角

Research progress on tRFs in the mechanisms of podocyte injury and apoptosis: new insights from the adriamycin nephropathy model

摘要:

慢性肾脏病（CKD）是重大公共卫生挑战，其核心病理是足细胞损伤。作为终末分化细胞，足细胞难以再生，成为CKD防治的关键靶点。阿霉素肾病（AN）模型可特异性诱导足细胞损伤，模拟人类CKD的蛋白尿与肾小球硬化特征。tRNA衍生片段（tRFs）作为新型非编码RNA，在足细胞损伤中起重要调控作用。该文综述了tRF-003634、tRF-013354、tRF-011690等通过调控TLR4/NF-κB、Wnt/β-catenin等信号通路诱导足细胞炎症、凋亡与骨架重构的机制。相关研究不仅揭示了tRFs在足细胞损伤中的新功能，也为理解CKD发病机制提供了新视角，并提示其作为生物标志物和潜在治疗靶点的价值与挑战。

Abstract:

Chronic kidney disease (CKD) represents a major public health challenge, and its core pathological feature is podocyte injury. As terminally differentiated cells, podocytes are difficult to regenerate, making them a critical target for CKD prevention and treatment. The adriamycin-induced nephropathy (AN) model specifically induces podocyte injury, effectively mimicking key characteristics of human CKD, including proteinuria and glomerulosclerosis. Recent studies have identified transfer RNA-derived fragments (tRFs) as a novel class of non-coding RNAs that play important regulatory roles in podocyte injury. This review summarizes the mechanisms by which specific tRFs, such as tRF-003634, tRF-013354 and tRF-011690, mediate podocyte inflammation, apoptosis, and cytoskeletal remodeling through the modulation of signaling pathways including TLR4/NF-κB and Wnt/β-catenin. These findings reveal new functions of tRFs, provide insights into the pathogenesis of CKD, and highlight both the value and the challenges of their application as biomarkers and therapeutic targets.