Evidence map›Paper›PMID 39696303›Full record

ArticleJournal of nanobiotechnology2024

Adipose-derived exosomes ameliorate skeletal muscle atrophy via miR-146a-5p/IGF-1R signaling.

Mengran Qin, Jiahao Zhu, Lipeng Xing, Yaotian Fan, Junyi Luo, Jiajie Sun, Ting Chen, Yongliang Zhang, Qianyun Xi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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

9 authors.

Mengran Qin *State Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Jiahao Zhu *State Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Lipeng Xing *State Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Yaotian Fan *State Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Junyi LuoState Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Jiajie SunState Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Ting ChenState Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Yongliang ZhangState Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China.
Qianyun XiState Key Laboratory of Livestock and Poultry Breeding, Guangdong Provincial Key Laboratory of Animal Nutrition Control, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, No. 483 Wushan Road, Guangzhou, 510642, China. xqy0228@scau.edu.cn.

Funding

National Natural Science Foundation of China 31802156National Natural Science Foundation of China 32072814
6 · The paper itself

Abstract

The study of muscle disorders has gained popularity, with a particular emphasis on the relationship between adipose tissue and skeletal muscle. In our investigation, we discovered that the deletion of miR-146a-5p specifically in adipose tissue (aKO) led to a notable rise in mice's mass and adiposity. In contrast, it led to a decline in lean mass, ability to exercise, diameter of muscle fibers, and the levels of genes associated with differentiation. The co-culture experiment showed that the transfection of miR-146a-5p mimics to 3T3-L1 significantly suppressive cell growth and promotes myotube differentiation in C2C12 cells. Exosomes from white adipose tissue (WAT) of aKO mice (aKO-WAT-Exos) significantly promoted muscle atrophy and inhibited differentiation of C2C12 cells but were reversed by co-incubation with miR-146a-5p-mimics. The miR-146a-5p can specifically target IGF-1R to improve skeletal muscle wasting. In this process, the PI3K/AKT/mTOR pathway is activated or the FoxO3 pathway is inhibited to enhance the synthesis of skeletal muscle proteins. Significantly, miR-146a-5p serves a crucial function as a microRNA in the communication of the fat-muscle connection. It can be transported through the pathway of exosomes derived from adipose tissue, ultimately ameliorating skeletal muscle atrophy and modulating body mass index (BMI).

Indexed as

ExosomesMicroRNAsMuscle, SkeletalMuscular AtrophyReceptor, IGF Type 1Signal Transduction3T3-L1 CellsAdipose TissueAdipose Tissue, WhiteAnimalsCell DifferentiationCell LineMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesIgf1r protein, mouseMicroRNAsMirn146 microRNA, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, IGF Type 1TOR Serine-Threonine KinasesAdiposeExosomesIGF-1RmiR-146a-5pMuscle atrophySkeletal muscle

Identifiers

PMID39696303
PMCPMC11657514

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.