Evidence map›Paper›PMID 38272853›Full record

ArticleJournal of cachexia, sarcopenia and muscle2024

CREG1 deficiency impaired myoblast differentiation and skeletal muscle regeneration.

Haixu Song, Xiaoxiang Tian, Lianqi He, Dan Liu, Jiayin Li, Zhu Mei, Ting Zhou, Chunying Liu, Jiaqi He, Xiaodong Jia and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

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  12. IL-33-Induced TREM2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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

13 authors at 1 institution in 1 country.

Haixu SongDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Xiaoxiang TianDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Lianqi HeDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Dan LiuDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Jiayin LiDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Zhu MeiDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Ting ZhouDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Chunying LiuDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Jiaqi HeDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Xiaodong JiaDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Zheming YangDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Chenghui YanDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.
Yaling HanDepartment of Cardiology, Cardiovascular Research Institute, State Key Laboratory of Frigid Zone Cardiovascular Disease, General Hospital of Northern Theater Command, Shenyang, China.ORCID 0000-0003-4569-6737
General Hospital of Shenyang Military Region · CN

Funding

Applied Basic Research Program of Liaoning Province 2022JH2/101300012Applied Basic Research Program of Liaoning Province 2022JH2/101500038Foundation Strengthening Plan Technical Field Fund Project 2021-JCJQ-JJ-1080National Science Funding of China 32071116National Science Funding of China 82070300National Science Funding of China 82070875National Science Funding of China 82270449National Science Funding of China 82270493
6 · The paper itself

Abstract

backgroundCREG1 (cellular repressor of E1A-stimulated genes 1) is a protein involved in cellular differentiation and homeostasis regulation. However, its role in skeletal muscle satellite cells differentiation and muscle regeneration is poorly understood. This study aimed to investigate the role of CREG1 in myogenesis and muscle regeneration.

methodsRNA sequencing data (GSE8479) was analysed from the Gene Expression Omnibus database (GEO, https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi). We generated Creg1 knockdown and skeletal muscle satellite cells specific Creg1 overexpression mice mediated by adeno-associated virus serotype 9 (AAV9), skeletal muscle mature myofibre Creg1 knockout mice (myoblast/Creg1MKO), and control mice Creg1

resultsWe analysed the transcriptional profiles of the skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women in GSE8479 database, and the results showed that Creg1 was associated with human sarcopenia. We found that Creg1 knockdown mice regenerated less newly formed fibres in response to cardiotoxin injection (~30% reduction, P < 0.01); however, muscle satellite cells specific Creg1 overexpression mice regenerated more newly formed fibres (~20% increase, P < 0.05). AMPKa1 is known as a key mediator in the muscle regeneration process. Our results revealed that CREG1 deficiency inhibited AMPKa1 signalling through C-CBL E3-ubiquitin ligase-mediated AMPKa1 degradation (P < 0.01). C-CBL-mediated AMPKa1 ubiquitination was attributed to the K48-linked polyubiquitination of AMPKa1 at K396 and that the modification played an important role in the regulation of AMPKa1 protein stability. We also found that Creg1MKO mice regenerated less newly formed fibres compared with Creg1

conclusionsOur findings suggest that CREG1 may be a potential therapeutic target for skeletal muscle regeneration.

Indexed as

CardiotoxinsMuscle, SkeletalAdultAnimalsCell DifferentiationFemaleHumansMaleMiceMyoblastsRegenerationRepressor ProteinsCardiotoxinsCREG1 protein, humanCreg protein, mouseRepressor ProteinsAMPKa1C‐CBLCREG1Satellite cellsSkeletal muscle regeneration

Identifiers

PMID38272853
PMCPMC10995283
OpenAlexW4391238159

What Socratic 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 Socratic graph.