A tRNA-derived fragment tiRNA-Met-CAT-002 induced by myocardial ischemia/reperfusion injury inhibits cardiomyocyte autophagy by regulating Bnip3

IF 3.5 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2025-10-22 DOI:10.1016/j.yexcr.2025.114809

Lang Deng , Yawen Weng , Jiahui Lin , Lingfeng Zhong , Zhixuan Tang , Shuang Lin , Weijian Huang , Zhenfeng Cheng , Kongjie Lu , Bozhi Ye

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Abstract

Myocardial ischemia/reperfusion (I/R) injury is a significant contributor to the development of heart failure. This study investigates the differential expression of tRNA-derived small RNAs (tsRNAs) during I/R and explores their potential functional implications. Through tRF & tiRNA sequencing, we identified 115 tsRNAs exhibiting significant changes in expression following I/R. Notably, tiRNA-Met-CAT-002 was found to be upregulated via the hypoxia/hypoxia-inducible factor 1 subunit α (HIF1α)/angiogenin (ANG) signaling axis. Our findings suggest that Bnip3 represents a crucial target for tiRNA-Met-CAT-002. Mechanistically, mimics of tiRNA-Met-CAT-002 reduced Bnip3 protein expression by directly targeting the 3′ untranslated region (UTR) of its mRNA in a manner resembling microRNA activity. Furthermore, tiRNA-Met-CAT-002 was observed to decrease autophagy levels while enhancing cell viability under hypoxia/reoxygenation (H/R) conditions. In conclusion, this study underscores the substantial role of tsRNAs in the pathophysiology of I/R injury, with tiRNA-Met-CAT-002 potentially serving as a protective factor by attenuating autophagy levels.

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心肌缺血/再灌注损伤诱导的trna衍生片段tiRNA-Met-CAT-002通过调节Bnip3抑制心肌细胞自噬

心肌缺血/再灌注（I/R）损伤是心衰发生的重要因素。本研究研究了trna衍生的小rna （tsrna）在I/R过程中的差异表达，并探讨了其潜在的功能意义。通过tRF &； tiRNA测序，我们鉴定出115种tsrna在I/R后表现出显著的表达变化。值得注意的是，tiRNA-Met-CAT-002通过缺氧/缺氧诱导因子1亚单位α (HIF1α)/血管生成素（ANG）信号轴被发现上调。我们的研究结果表明Bnip3是tiRNA-Met-CAT-002的关键靶点。在机制上，模拟tiRNA-Met-CAT-002通过直接靶向其mRNA的3 '非翻译区（UTR），以类似于microRNA活性的方式降低Bnip3蛋白的表达。此外，在缺氧/再氧化（H/R）条件下，观察到tiRNA-Met-CAT-002可以降低自噬水平，同时提高细胞活力。总之，本研究强调了tsRNAs在I/R损伤病理生理中的重要作用，其中tiRNA-Met-CAT-002可能通过降低自噬水平作为一种保护因子。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Experimental cell research 医学-细胞生物学

CiteScore

7.20

自引率

0.00%

发文量

295

审稿时长

30 days

期刊介绍： Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.