Screening and Evaluation of tRF-Glu-CTC-013 as a Biomarker and Key Regulator in the Development of Cardiac Hypertrophy

作者：Wenlin Li, Ming Lan, Kun Xu, Sainan Li, Que Wang, Beidong Chen, Xiuqing Huang, Lin Dou, Na Jia, Li Zhao, Yuefeng Wang, Xingyun Jiao, Yong Man, Deping Liu, Liang Sun, Tong Zou, Qing He, Jian Li, Xue Yu, Tao Shen · 发表于：International Journal of Medical Sciences · 年份：2025 · DOI：10.7150/ijms.106114 · 被引用次数：5 · 研究领域：Cardiovascular Function and Risk Factors、Cardiomyopathy and Myosin Studies、Cardiac Fibrosis and Remodeling

tRNA-derived small RNAs (tsRNAs) are a newly recognized class of non-coding RNAs involved in regulating RNA processing and translational control. Pathological cardiac hypertrophy, characterized by left ventricular remodeling under chronic stress, serves as a critical precursor to severe cardiovascular pathologies including myocardial ischemia, infarction, and heart failure. Utilizing an angiotensin II (Ang II)-induced mouse cardiac hypertrophy model combined with tsRNA transcriptome profiling, we identified differentially expressed tsRNAs and investigated their functional relevance. Validation in neonatal mouse ventricular myocytes (NMVMs) revealed five upregulated tsRNAs associated with hypertrophic progression. Functional characterization showed that overexpressing tRF-Glu-CTC-013 significantly reduced cardiomyocyte hypertrophy and inhibited inflammation and fibrosis. Further luciferase reporter assays revealed that tRF-Glu-CTC-013 could bind to the 3' UTR of TAS1R3, thereby inhibiting its expression and enhancing the level of autophagy in NMVMs. Taken together, these findings suggest that tsRNAs may act as novel regulators of cardiac remodeling, with tRF-Glu-CTC-013 emerging as a promising therapeutic candidate for cardioprotection via anti-hypertrophic, anti-inflammatory, and anti-fibrotic mechanisms.