Evidence map›Paper›PMID 38010513›Full record

ArticleCellular and molecular life sciences : CMLS2023

Interleukin 4 improved adipose-derived stem cells engraftment via interacting with fibro/adipogenic progenitors in dystrophic mice.

Huan Li, Jinfu Lin, Liang Wang, Ruojie He, Jing Li, Menglong Chen, Weixi Zhang, Cheng Zhang

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

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. 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

8 authors at 3 institutions in 1 country.

Huan LiDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China.
Jinfu LinDepartment of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, 515000, China.
Liang WangDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China.
Ruojie HeDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China.
Jing LiDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China.
Menglong ChenDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510080, China.
Weixi ZhangDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China. zhangwxi@mail.sysu.edu.cn.
Cheng ZhangDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou, 510080, China. chengzhang100@foxmail.com.ORCID http://orcid.org/0000-0003-1934-528X
Sun Yat-sen University · CNFirst Affiliated Hospital of Jinan University · CNShantou University · CN

Funding

Guangdong Provincial Clinical Research Center for Neurological Diseases of Chinese Medicine, Guangzhou University of Chinese Medicine 2020B1111170002Guangdong Provincial Engineering Center for Major Neurological Disease Treatment, Guangdong Provincial Translational Medicine Innovation Platform for Diagnosis and Treatment of Major Neurological Disease, Guangzhou Clinical Research and Translational Cente 201604020010Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases 2020B1212060017Natural Science Foundation of China 81471280Natural Science Foundation of China 81771359Science and Technology Planning Project of Guangdong 2021A1515010313Southern China International Joint Research Center for Early Intervention and Functional Rehabilitation of Neurological Diseases 2015B050501003Southern China International Joint Research Center for Early Intervention and Functional Rehabilitation of Neurological Diseases 2020A0505020004
6 · The paper itself

Abstract

Adipose-derived stem cells (ADSC) therapy shows promise as an effective treatment for dystrophinopathy. Fibro-/adipogenic progenitors (FAPs) play an essential role in the myogenesis of muscle satellite cells and contribute to muscle fibrosis and adipocyte infiltration. The interleukin 4 (IL-4) pathway acts as a switch that regulates the functions of FAPs. The interaction between FAPs and engrafted cells remains unclear. In this study, we used a co-culture system to investigate possible crosstalk between the FAPs of dystrophic mice and ADSC overexpressing IL4 (IL4-ADSC) and control ADSC. Systemic transplantation of IL4-ADSC and control ADSC in dystrophic mice was conducted for 16 weeks, after which motor function and molecular improvements were evaluated. Overexpression of IL4 in ADSC significantly promoted myogenesis in vitro, increasing the expression of Pax7, Myogenin, and MyHC. Co-culture indicated that although myoblasts derived from control ADSC promoted adipogenic and fibrogenic differentiation of FAPs, FAPs did not significantly affect myogenesis of ADSC-derived myoblasts. However, overexpression of IL4 in ADSC inhibited their myotube-dependent promotion of FAPs differentiation on the one hand and promoted FAPs to enhance myogenesis on the other. Dystrophic mice administered with IL4-ADSC-derived myoblasts displayed significantly better motor ability, more engrafted cells showing dystrophin expression, and less muscle fibrosis, intramuscular adipocytes, and macrophage infiltration than mice administered control-ADSC-derived myoblasts. In conclusion, IL4 activation enhanced the therapeutic potential of ADSC transplantation in dystrophic mice, possibly by improving the myogenesis of IL4-ADSC and altering the crosstalk between engrafted stem cells and resident FAPs.

Indexed as

Interleukin-4Satellite Cells, Skeletal MuscleAdipogenesisAnimalsCell DifferentiationFibrosisMiceMuscle, SkeletalStem CellsInterleukin-4Adipose-derived stem cellsDystrophinopathyFibro-/adipogenic progenitorsIL4Muscle fibrosis

Identifiers

PMID38010513
PMCPMC10682070
OpenAlexW4389048714

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.