ArticleInternational journal of medical sciences2025
Screening and Evaluation of tRF-Glu-CTC-013 as a Biomarker and Key Regulator in the Development of Cardiac Hypertrophy.
Article in International journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Transfer RNA-derived small RNAs in cardiovascular diseases: Progress and perspectives.Non-coding RNA research · 2026Review
- tsRNA-3025a Impairs Mitochondrial Function and Autophagy to Inhibit Myocardial Regeneration and Repair Following Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2026Article
- Regulatory Roles of Mitochondrial tRNA-Derived Fragments in Cardiovascular Health and Disease.Journal of the American Heart Association · 2025Review
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.