Evidence map›Paper›PMID 37270528›Full record

ArticleBiological research2023

iPSCs ameliorate hypoxia-induced autophagy and atrophy in C2C12 myotubes via the AMPK/ULK1 pathway.

Haimei Cen, Pin Fan, Yuting Ding, Bin Luo, Hong Luo, Menglong Chen, Yu Zhang

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Haimei CenDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Pin FanDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Yuting DingDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Bin LuoDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China.
Hong LuoDepartment of Neurology, Meizhou People's Hospital, Meizhou, 514000, Guangdong, China.
Menglong ChenDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China. cmlcalm@sina.com.
Yu ZhangDepartment of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, Guangdong, China. yuzhang2016@jnu.edu.cn.ORCID http://orcid.org/0000-0003-3239-3796
First Affiliated Hospital of Jinan University · CNMeizhou City People's Hospital · CN

Funding

National Natural Science Foundation of China 81801246
6 · The paper itself

Abstract

backgroundDuchenne muscular dystrophy (DMD) is an X-linked lethal genetic disorder for which there is no effective treatment. Previous studies have shown that stem cell transplantation into mdx mice can promote muscle regeneration and improve muscle function, however, the specific molecular mechanisms remain unclear. DMD suffers varying degrees of hypoxic damage during disease progression. This study aimed to investigate whether induced pluripotent stem cells (iPSCs) have protective effects against hypoxia-induced skeletal muscle injury.

resultsIn this study, we co-cultured iPSCs with C2C12 myoblasts using a Transwell nested system and placed them in a DG250 anaerobic workstation for oxygen deprivation for 24 h. We found that iPSCs reduced the levels of lactate dehydrogenase and reactive oxygen species and downregulated the mRNA and protein levels of BAX/BCL2 and LC3II/LC3I in hypoxia-induced C2C12 myoblasts. Meanwhile, iPSCs decreased the mRNA and protein levels of atrogin-1 and MuRF-1 and increased myotube width. Furthermore, iPSCs downregulated the phosphorylation of AMPKα and ULK1 in C2C12 myotubes exposed to hypoxic damage.

conclusionsOur study showed that iPSCs enhanced the resistance of C2C12 myoblasts to hypoxia and inhibited apoptosis and autophagy in the presence of oxidative stress. Further, iPSCs improved hypoxia-induced autophagy and atrophy of C2C12 myotubes through the AMPK/ULK1 pathway. This study may provide a new theoretical basis for the treatment of muscular dystrophy in stem cells.

Indexed as

AMP-Activated Protein KinasesInduced Pluripotent Stem CellsAnimalsAtrophyAutophagyHypoxiaMiceMice, Inbred mdxMuscle Fibers, SkeletalMuscle, SkeletalRNA, MessengerAMP-Activated Protein KinasesRNA, MessengerAMPK/ULK1 pathwayAtrogin-1Co-cultureDuchenne muscular dystrophyHypoxiaLC3II/LC3IMuRF-1

Identifiers

PMID37270528
PMCPMC10239182
OpenAlexW4379207658

What OpenQuestion holds

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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.