Evidence map›Paper›PMID 34909122›Full record

ArticleWorld journal of stem cells2021

Exosomes derived from inflammatory myoblasts promote M1 polarization and break the balance of myoblast proliferation/differentiation.

Zhi-Wen Luo, Ya-Ying Sun, Jin-Rong Lin, Bei-Jie Qi, Ji-Wu Chen

Open access · hybridAbstract read
In one paragraph

Article in World journal of stem cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  10. Exosomes and microRNAs as mediators of the exercise.European journal of medical research · 2025
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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

5 authors at 3 institutions in 1 country.

Zhi-Wen LuoDepartment of Sports Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Ya-Ying SunDepartment of Sports Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jin-Rong LinDepartment of Sports Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Bei-Jie QiDepartment of Sports Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Ji-Wu ChenDepartment of Sports Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Fudan University · CNHuashan Hospital · CNShanghai University of Sport · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute muscle injuries are one of the most common injuries in sports. Severely injured muscles are prone to re-injury due to fibrotic scar formation caused by prolonged inflammation. How to regulate inflammation and suppress fibrosis is the focus of promoting muscle healing. Recent studies have found that myoblasts and macrophages play important roles in the inflammatory phase following muscle injury; however, the crosstalk between these two types of cells in the inflammatory environment, particularly the exosome-related mechanisms, had not been well studied.

aimTo evaluate the effects of exosomes from inflammatory C2C12 myoblasts (IF-C2C12-Exos) on macrophage polarization and myoblast proliferation/differentiation.

methodsA model of inflammation was established

resultsWe found that the PKH-67-marked C2C12-Exos can be endocytosed by both macrophages and myoblasts. IF-C2C12-Exos induced M1 macrophage polarization and suppressed the M2 phenotype

conclusionIF-C2C12-Exos can induce M1 polarization, resulting in a sustained and aggravated inflammatory environment that impairs myoblast differentiation, and leads to enhanced myogenic proliferation. These results demonstrate why prolonged inflammation occurs after acute muscle injury and provide a new target for the regulation of muscle regeneration.

Indexed as

C2C12 myoblastDifferentiationExosomesInflammationMacrophage polarizationProliferation

Identifiers

PMID34909122
PMCPMC8641021
OpenAlexW3217625118

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.