Evidence map›Paper›PMID 34913989›Full record

ArticleDiabetologia2022

MicroRNA-193b impairs muscle growth in mouse models of type 2 diabetes by targeting the PDK1/Akt signalling pathway.

Shu Yang, Guangyan Yang, Han Wu, Lin Kang, Jiaqing Xiang, Peilin Zheng, Shanhu Qiu, Zhen Liang, Yan Lu, Lijing Jia

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Potential Therapeutic Strategies for Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022
    Review
  16. mRNA mCellular and molecular life sciences : CMLS · 2022
    Article
  17. 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

10 authors at 2 institutions in 1 country.

Shu YangDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.ORCID 0000-0002-4912-777X
Guangyan YangDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.
Han WuDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.
Lin KangDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.
Jiaqing XiangDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.
Peilin ZhengDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.ORCID 0000-0002-4712-4903
Shanhu QiuDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China.
Zhen LiangDepartment of Geriatrics, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China. liang.zhen@szhospital.com.ORCID 0000-0003-4700-0203
Yan LuDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China. lu.yan2@zs-hospital.sh.cn.
Lijing JiaDepartment of Endocrinology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Shenzhen, China. jialijing2012@126.com.
Jinan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisType 2 diabetes is associated with a reduction in skeletal muscle mass; however, how the progression of sarcopenia is induced and regulated remains largely unknown. We aimed to find out whether a specific microRNA (miR) may contribute to skeletal muscle atrophy in type 2 diabetes.

methodsAdeno-associated virus (AAV)-mediated skeletal muscle miR-193b overexpression in C57BLKS/J mice, and skeletal muscle miR-193b deficiency in db/db mice were used to explore the function of miR-193b in muscle loss. In C57BL/6 J mice, tibialis anterior-specific deletion of 3-phosphoinositide-dependent protein kinase-1 (PDK1), mediated by in situ AAV injection, was used to confirm whether miR-193b regulates muscle growth through PDK1. Serum miR-193b levels were also analysed in healthy individuals (n = 20) and those with type 2 diabetes (n = 20), and correlations of miR-193b levels with HbA

resultsIn this study, we found that serum miR-193b levels increased in individuals with type 2 diabetes and negatively correlated with muscle mass in these participants. Functional studies further showed that AAV-mediated overexpression of miR-193b induced muscle loss and dysfunction in healthy mice. In contrast, suppression of miR-193b attenuated muscle loss and dysfunction in db/db mice. Mechanistic analysis revealed that miR-193b could target Pdk1 expression to inactivate the Akt/mammalian target of rapamycin (mTOR)/p70S6 kinase (S6K) pathway, thereby inhibiting protein synthesis. Therefore, knockdown of PDK1 in healthy mice blocked miR-193b-induced inactivation of the Akt/mTOR/S6K pathway and impairment of muscle growth. CONCLUSIONS/

interpretationOur results identified a previously unrecognised role of miR-193b in muscle function and mass that could be a potential therapeutic target for treating sarcopenia.

Indexed as

Diabetes Mellitus, Type 2MicroRNAsAnimalsMammalsMiceMice, Inbred C57BLMuscle, SkeletalProto-Oncogene Proteins c-aktMicroRNAsProto-Oncogene Proteins c-aktAktmiR-193bMuscles atrophyPDK1Type 2 diabetes

Identifiers

PMID34913989
PMCPMC8803817
OpenAlexW4200320056

What OpenQuestion holds

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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.