ArticleMolecular medicine reports2025
A novel tRNA‑derived small RNA, 5'tiRNA‑Gln‑TTG‑001, aggravates cardiomyocyte inflammatory injury through upregulation of CLIC4.
Article in Molecular medicine reports, 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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Who cites it
3 citing papers in PubMed.
- Transfer RNA-derived small RNAs in cardiovascular diseases: Progress and perspectives.Non-coding RNA research · 2026Review
- Biological functions of tsRNAs and research advances in human disease.Biochemistry and biophysics reports · 2026Review
- Anti-Inflammatory and Protective Role of tiRNA-Glu-TTC-003 in Pediatric Sepsis Via TREM2/TLR4 Signaling Modulation.Inflammation · 2026Article
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Authors and funding
5 authors.
Funding
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Abstract
Acute myocarditis encompasses a spectrum of diseases characterized by ongoing inflammation and cardiomyocyte injury, lacking specific diagnostic biomarkers and effective therapies. Transfer RNA (tRNA)‑derived small RNAs (tsRNAs), formed by specific cleavage of tRNAs in response to certain stimuli, participate in diverse diseases; however, their involvement in myocarditis remains unclear. The present study aimed to investigate the role and mechanism of a novel tsRNA, 5'tRNA‑derived stress‑induced RNA (tiRNA)‑Gln‑TTG‑001, in myocarditis. Plasma samples were obtained from patients with acute myocarditis to examine the clinical significance of 5'tiRNA‑Gln‑TTG‑001. AC16 human cardiomyocytes treated with lipopolysaccharide to induce inflammatory responses were utilized to explore the function and mechanism of 5'tiRNA‑Gln‑TTG‑001. Cell viability, apoptosis rates, and levels of factors associated with inflammation (IL‑1β, IL‑6 and IL‑18), myocardial injury (creatine kinase MB and high‑sensitivity cardiac troponin) and myocardial dysfunction (N‑terminal pro‑B‑type natriuretic peptide) were quantified to assess the degree of cardiomyocyte inflammatory injury. RNA fluorescence
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