Evidence map›Paper›PMID 35013149›Full record

ArticleCell death discovery2022

tRNA-derived fragment TRF365 regulates the metabolism of anterior cruciate ligament cells by targeting IKBKB.

Dianbo Long, Yiyang Xu, Guping Mao, Ruobing Xin, Zengfa Deng, Hongyi Liao, Zhiwen Li, Zhi Yang, Baoxi Yu, Zhijian Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  7. Astaxanthin mediated repair of tBHP-Induced cellular injury in chondrocytes.Redox report : communications in free radical research · 2024
    Article
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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

13 authors at 2 institutions in 1 country.

Dianbo Long *Department of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Yiyang Xu *Department of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Guping Mao *Department of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Ruobing XinDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Zengfa DengDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Hongyi LiaoDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Zhiwen LiDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Zhi YangDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Baoxi YuDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Zhijian YangDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Aishan HeDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China. heaishan@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0003-0629-1390
Ziji ZhangDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China. zhangziji@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7040-8576
Yan KangDepartment of Joint Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China. kangyan2@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-6233-0652
Sun Yat-sen University · CNFujian Medical University · CN

Funding

China Postdoctoral Science Foundation 2019M663263China Postdoctoral Science Foundation 2020M683085National Natural Science Foundation of China (National Science Foundation of China) 81874014National Natural Science Foundation of China (National Science Foundation of China) 81972051Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2019A1515011946Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2020A1515110943Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2021A1515010454
6 · The paper itself

Abstract

tRNA-derived fragments (tRFs) are new noncoding RNAs, and recent studies have shown that tRNAs and tRFs have important functions in cell metabolism via posttranscriptional regulation of gene expression. However, whether tRFs regulate cellular metabolism of the anterior cruciate ligament (ACL) remains elusive. The aim of this study was to investigate the role and action mechanism of tRFs in ACL cell metabolism. A tRF array was used to determine tRF expression profiles in different human ACL cells, and quantitative real-time polymerase chain reaction and fluorescence in situ hybridisation were used to determine TRF365 expression. ACL cells were transfected with a TRF365 mimic or a TRF365 inhibitor to determine whether TRF365 regulates IKBKB expression. A rescue experiment and dual-luciferase reporter assay were conducted to determine whether the 3'-untranslated region (UTR) of IKBKB has a TRF365-binding site. TRF365 was weakly expressed in osteoarthritis (OA) ACL and interleukin-1β-treated ACL cells. IKBKB was highly expressed in OA ACL and interleukin-1β-treated ACL cells; transfection with the TRF365 mimic suppressed IKBKB expression, whereas transfection with the TRF365 inhibitor had the opposite effect. A dual-luciferase reporter assay showed that TRF365 silenced the expression of IKBKB by binding to its 3'-UTR. Thus, TRF365 regulates the metabolism of ACL cells by targeting IKBKB. In summary, TRF365 may provide a new direction for the study of ACL degeneration and on the pathophysiological process of OA.

Identifiers

PMID35013149
PMCPMC8748987
OpenAlexW4205574896

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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.