Evidence map›Paper›PMID 34606978›Full record

ArticleJournal of sport and health science2022

Exercise promotes angiogenesis by enhancing endothelial cell fatty acid utilization via liver-derived extracellular vesicle miR-122-5p.

Jing Lou, Jie Wu, Mengya Feng, Xue Dang, Guiling Wu, Hongyan Yang, Yan Wang, Jia Li, Yong Zhao, Changhong Shi and 4 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of sport and health science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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1 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

14 authors at 2 institutions in 1 country.

Jing LouCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Jie WuSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China; Medical School of Chinese PLA, Beijing 100853, China.
Mengya FengCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Xue DangSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Guiling WuSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Hongyan YangSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Yan WangCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Jia LiSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Yong ZhaoLaboratory Animal Center, Fourth Military Medical University, Xi'an 710032, China.
Changhong ShiLaboratory Animal Center, Fourth Military Medical University, Xi'an 710032, China.
Jiankang LiuCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Lin ZhaoCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: zhaolin2015@mail.xjtu.edu.cn.
Xing ZhangSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China. Electronic address: zhangxing@fmmu.edu.cn.
Feng GaoSchool of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Air Force Medical University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiogenesis constitutes a major mechanism responsible for exercise-induced beneficial effects. Our previous study identified a cluster of differentially expressed extracellular vesicle microRNAs (miRNAs) after exercise and found that some of them act as exerkines. However, whether these extracellular vesicle miRNAs mediate the exercise-induced angiogenesis remains unknown.

methodsA 9-day treadmill training was used as an exercise model in C57BL/6 mice. Liver-specific adeno-associated virus 8 was used to knock down microRNA-122-5p (miR-122-5p). Human umbilical vein endothelial cells were used in vitro.

resultsAmong these differentially expressed extracellular vesicle miRNAs, miR-122-5p was identified as a potent pro-angiogenic factor that activated vascular endothelial growth factor signaling and promoted angiogenesis both in vivo and in vitro. Exercise increased circulating levels of miR-122-5p, which was produced mainly by the liver and shuttled by extracellular vesicles in mice. Inhibition of circulating miR-122-5p or liver-specific knockdown of miR-122-5p significantly abolished the exercise-induced pro-angiogenic effect in skeletal muscles, and exercise-improved muscle performance in mice. Mechanistically, miR-122-5p promoted angiogenesis through shifting substrate preference to fatty acids in endothelial cells, and miR-122-5p upregulated endothelial cell fatty-acid utilization by targeting 1-acyl-sn-glycerol-3-phosphate acyltransferase (AGPAT1). In addition, miR-122-5p increased capillary density in perilesional skin tissues and accelerated wound healing in mice.

conclusionThese findings demonstrated that exercise promotes angiogenesis through upregulation of liver-derived extracellular vesicle miR-122-5p, which enhances fatty acid utilization by targeting AGPAT1 in endothelial cells, highlighting the therapeutic potential of miR-122-5p in tissue repair.

Indexed as

Extracellular VesiclesMicroRNAsNeovascularization, PhysiologicPhysical Conditioning, AnimalAnimalsFatty AcidsHumansHuman Umbilical Vein Endothelial CellsLiverMiceMice, Inbred C57BLVascular Endothelial Growth Factor AFatty AcidsMicroRNAsMIRN122 microRNA, humanMirn122 microRNA, mouseVascular Endothelial Growth Factor AAngiogenesisEndothelial cellsExerkineExtracellular vesicleMetabolic shift

Identifiers

PMID34606978
PMCPMC9338338
OpenAlexW3202884287

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.