Evidence map›Paper›PMID 40399722›Full record

ArticleCell biology and toxicology2025

A novel tsRNA signature -tRF-58:76-Tyr-GTA-2-M3 as potential biomarker and therapeutic target for duodenal atresia.

Xinyue Meng, Xiaowei Wei, Hui Gu, Wei Ma, Dan Liu, Shanshan Jia, Songying Cao, Dongxue Ding, Yiwen He, Wanqi Huang and 4 more

Abstract read
In one paragraph

Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Xinyue MengDepartment of Ultrasound, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Xiaowei WeiKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Hui GuKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Wei MaKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Dan LiuKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Shanshan JiaKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Songying CaoKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Dongxue DingKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Yiwen HeKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Wanqi HuangKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Jia XueKey Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China.
Wenting Luo *Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China. lvirginia@163.com.
Wei Sun *Department of Ultrasound, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China. sunwei8677@126.com.
Zhengwei Yuan *Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning, China. yuanzw@hotmail.com.

Funding

Applied basic research program for young scholars of Liaoning Province 2023JH2/101600026LiaoNing Revitalization Talents Program XLYC1902099National Key Research and Development Program No.2021YFC2701003National Natural Science Foundation of China 82171649National Natural Science Foundation of China 82402313The Science and Technology Plan Joint Plan Project of Liaoning Province 2024-BSLH-317the Science and Technology Plan Project of Liaoning Province 2023JH2/20200082
6 · The paper itself

Abstract

Duodenal atresia (DA) is a common neonatal digestive tract obstruction, with unclear prenatal diagnostic specificity and optimal intervention timing. tRNA-derived small RNAs (tsRNAs), stable and enriched in blood, are promising biomarkers for disease diagnosis. Therefore, identifying tsRNA biomarkers, elucidating DA pathogenesis, and exploring potential intrauterine interventions is urgently needed. This study conducts tsRNA profiling via sequencing on plasma samples from pregnant women carrying fetuses with DA and matched healthy controls. Validation was performed in 147 pregnant women, including cohorts with fetal gastrointestinal atresia, normal pregnancies, and post-delivery cases. Functional analyses in cellular models and Adriamycin rat models with DA explored the role of key tsRNAs in DA pathogenesis and intrauterine therapy. It is found that tsRNAs, including tRF-61:78-chrM. Leu-TAA, tRF-60:77-Ile-AAT-1-M4, tRF-57:76-Arg-ACG-1-M2, and tRF-58:76-Tyr-GTA-2-M3, were significantly downregulated in DA cases. tRF-58:76-Tyr-GTA-2-M3 is further implicated in DA development, with knockdown inducing excessive apoptosis via upregulation of SUFU and suppression of GLI1, a hedgehog pathway transcription factor. Intraperitoneal microinjection of tRF-58:76-Tyr-GTA-2-M3 agomir in DA rat models reduce apoptosis and mitigates DA formation by modulating SUFU and GLI1 expression. Taken together, this study identifies novel tsRNA biomarkers for DA, with tRF-58:76-Tyr-GTA-2-M3 playing a pivotal role in its pathogenesis. These findings offer insights into DA mechanisms and suggest potential therapeutic targets, advancing strategies for early diagnosis and intervention.

Indexed as

Duodenal ObstructionIntestinal AtresiaRNA, TransferAdultAnimalsBiomarkersCase-Control StudiesDisease Models, AnimalFemaleHumansPregnancyRatsRats, Sprague-DawleyBiomarkersRNA, TransferApoptosisDuodenal atresiaIntrauterine treatmentPlasma biomarkerTRNA-derived small RNAs

Identifiers

PMID40399722
PMCPMC12095417

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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 OpenQuestion graph.