Evidence map›Paper›PMID 41612654›Full record

ArticleJournal of cachexia, sarcopenia and muscle2026

EIF4A3-Induced Circular RNA circSnd1 Promotes Muscle Atrophy and Muscle Ageing by Stabilizing EEF1A1.

Jin Li, Bing Jin, Yuwei Yan, Yuying Chen, Xiaohang Yin, Xinyi Ren, Qian Li, Jingying Chen, Siqi Wang, Tingting Yang and 12 more

Abstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2026. 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. Article
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

22 authors.

Jin LiCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Bing JinCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Yuwei YanCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Yuying ChenCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Xiaohang YinCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Xinyi RenCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Qian LiCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Jingying ChenCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Siqi WangCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Tingting YangCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Yanan ZhangCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Qiumeng NieCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.
Dongchao LuSchool of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Ming WuDepartment of Orthopedics, Shanghai Gongli Hospital, Shanghai, China.
Yan YuDepartment of Spine Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Lei ChenDepartment of Spine Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Tarun KeswaniCenter for Immunological and Inflammatory Diseases, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Guoping LiCardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Dragos CretoiuDepartment of Medical Genetics, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
T Scott BowenSchool of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
Junjie XiaoCardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong) and School of Life Sciences, Shanghai University, Nantong, China.ORCID https://orcid.org/0000-0002-9202-0003
Yongjun ZhengDivision of Pain Management, Huadong Hospital Affiliated to Fudan University, Shanghai, China.

Funding

National Key R&D Program of China 2020YFA0803800National Natural Science Foundation of China 82020108002National Natural Science Foundation of China 82225005National Natural Science Foundation of China 82271623National Natural Science Foundation of China 82400423National Natural Science Foundation of China 82401851National Natural Science Foundation of China 82471618National Natural Science Foundation of China 825722922Science and Technology Commission of Shanghai Municipality 22010500200Science and Technology Commission of Shanghai Municipality 23410750100Science and Technology Commission of Shanghai Municipality 23ZR1420500Shanghai Pujiang Program 23PJ1412200Shanghai Rising-Star Program 23QA1403600
6 · The paper itself

Abstract

backgroundMuscle atrophy is a common complication of ageing, and many chronic conditions, lacks defined therapeutic interventions. It is still mostly unknown how circular RNAs contribute to muscle atrophy.

methodscircRNA sequencing and quantitative real-time PCR were performed to detect the changed circRNAs in muscle atrophy models and aged muscle. Then the gain-of-function and loss-of-function experiments were used to investigate the function of circSnd1 in muscle atrophy and muscle ageing. Furthermore, we used RIP-MS and RIP assay to determine the downstream and upstream mechanism of circSnd1 in muscle atrophy.

resultsHere, we characterized the function and mechanism of highly species-conserved circRNA derived from staphylococcal nuclease and Tudor domain containing 1 gene (named circSnd1) in muscle atrophy. CircSnd1 is upregulated in many types of muscle atrophy models in both in vivo and in vitro (all p < 0.01). Meanwhile, circSnd1 is also higher expressed in aged muscle in humans (+2.2-fold, n = 5, p < 0.05), mice (+43.96%, n = 6, p < 0.05) and myotubes (+42.21%, n = 6, p < 0.05). Functional analyses show that circSnd1 promotes muscle atrophy and muscle ageing at the cellular level and mouse level while repressing it ameliorates multiple types of muscle atrophy (all p < 0.05). Mechanistically, the RNA binding protein eukaryotic translation initiation factor 4A3 (EIF4A3) can bind to the intron flanking sequence of circSnd1 to induce circSnd1 cyclization and increase circSnd1 expression in muscle atrophy. In addition, circSnd1 promotes the binding between human HLA-F adjacent transcript 10 (FAT10) and eukaryotic translation elongation factor 1 alpha 1 (EEF1A1). FAT10 competes with ubiquitin for binding with EEF1A1, which decreases the ubiquitination of EEF1A1 and stabilizes the protein level of EEF1A1 in muscle cells to promote atrophy.

conclusionsWe have identified circSnd1 as a novel circRNA that promotes muscle atrophy and highlighted its potential as a novel therapeutic target.

Indexed as

AgingEukaryotic Initiation Factor-4AMuscular AtrophyPeptide Elongation Factor 1RNA, CircularAnimalsDEAD-box RNA HelicasesHumansMaleMiceMuscle, SkeletalDEAD-box RNA HelicasesEIF4A3 protein, humanEukaryotic Initiation Factor-4APeptide Elongation Factor 1RNA, CircularcircSnd1EEF1A1 ubiquitinationEIF4A3FAT10muscle ageingmuscle atrophy

Identifiers

PMID41612654
PMCPMC12855621

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.