Evidence map›Paper›PMID 29512357›Full record

ArticleJournal of cachexia, sarcopenia and muscle2018

A newly identified lncRNA MAR1 acts as a miR-487b sponge to promote skeletal muscle differentiation and regeneration.

Zong-Kang Zhang, Jie Li, Daogang Guan, Chao Liang, Zhenjian Zhuo, Jin Liu, Aiping Lu, Ge Zhang, Bao-Ting Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
8.0field-weighted citation impact, top 1% 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

114 citing papers in PubMed, 195 citations in OpenAlex.

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  13. Curcumin-activated Wnt5a pathway mediates CaJournal of cachexia, sarcopenia and muscle · 2024
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  14. Review
  15. Article
  16. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review
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54 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Zong-Kang ZhangSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Jie LiSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Daogang GuanInstitute of Integrated Bioinformedicine and Translational Science, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Chao LiangLaw Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Zhenjian ZhuoSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Jin LiuLaw Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Aiping LuInstitute of Integrated Bioinformedicine and Translational Science, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Ge ZhangLaw Sau Fai Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Bao-Ting ZhangSchool of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, China.
Hong Kong Baptist University · HKChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSkeletal muscle atrophy induced by either aging (sarcopenia) or mechanical unloading is associated with serious health consequences. Long non-coding RNAs (lncRNAs) are implicated as important regulators in numerous physiological and pathological processes.

methodsMicroarray analysis was performed to identify the differentially expressed lncRNAs in skeletal muscle between adult and aged mice. The most decreased lncRNA in aged skeletal muscle was identified. The C2C12 mouse myoblast cells were used to assess the biological function of the lncRNA in vitro. The target microRNA of lncRNA and the target protein of microRNA were predicted by bioinformatics analysis and validated in vitro. Furthermore, the biology function of the lncRNA in vivo was investigated by local overexpression or knockdown the lncRNA in skeletal muscle. The therapeutic effect of the lncRNA overexpression in age-related or mechanical unloading-induced muscle atrophy was also evaluated.

resultsWe identified a novel lncRNA (muscle anabolic regulator 1, MAR1) which was highly expressed in mice skeletal muscle and positively correlated with muscle differentiation and growth in vitro and in vivo. We predicted and validated that microRNA-487b (miR-487b) was a direct target of MAR1. We also predicted and validated that Wnt5a, an important regulator during myogenesis, was a target of miR-487b in C2C12 cells. Our findings further demonstrated that enforced MAR1 expression in myoblasts led to derepression of Wnt5a. Moreover, MAR1 promoted skeletal muscle mass/strength and Wnt5a protein level in mice. Enforced MAR1 expression in mice attenuated muscle atrophy induced by either aging or unloading.

conclusionsThe newly identified lncRNA MAR1 acts as a miR-487b sponge to regulate Wnt5a protein, resulting in promoting muscle differentiation and regeneration. MAR1 could be a novel therapeutic target for treating muscle atrophy induced by either aging or mechanical unloading.

Indexed as

AgingAnimalsCell DifferentiationCell LineMice, Inbred C57BLMicroRNAsMuscle DevelopmentMuscle, SkeletalMyoblastsRegenerationRNA, Long NoncodingWnt-5a ProteinMicroRNAsMIRN487 microRNA, mouseRNA, Long NoncodingWnt-5a ProteinWnt5a protein, mouseLong non-coding RNAmiR-487bMuscle differentiationMuscle regenerationWnt5a

Identifiers

PMID29512357
PMCPMC5989759
OpenAlexW2791574629

What OpenQuestion holds

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Registered trials

None linked

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.