Evidence map›Paper›PMID 37284884›Full record

ArticleThe Journal of experimental medicine2023

Myofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling.

Jingya Xu, Xiaofei Li, Wei Chen, Ziyin Zhang, Yanping Zhou, Yahui Gou, Cheng-An Lv, Lu Jin, Xinyuan Qiu, Shengshan Ma and 9 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 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

19 authors at 5 institutions in 2 countries.

Jingya Xu *Department of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0007-6196-0725
Xiaofei Li *Department of Sport Medicine, Xuzhou Medical University Affiliated Hospital of Lianyungang, Lianyungang, China.ORCID 0009-0002-0686-1859
Wei Chen *Department of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0002-9853-8049
Ziyin ZhangDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0000-1432-1321
Yanping ZhouDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0005-3974-5143
Yahui GouDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0001-2126-1811
Cheng-An LvDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0001-5998-4815
Lu JinDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0002-0946-3357
Xinyuan QiuDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0002-9662-8075
Shengshan MaDepartment of Sport Medicine, Xuzhou Medical University Affiliated Hospital of Lianyungang, Lianyungang, China.ORCID 0000-0003-1304-8786
Qing-Qian WuDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0001-7392-8801
Tongyu LiuDepartment of Cell and Developmental Biology, Life Sciences Institute, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0002-8579-2144
Lin MiDepartment of Cell and Developmental Biology, Life Sciences Institute, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0001-9157-578X
Zhuoying YangDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0004-3784-0043
Ting YuDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0009-0006-4266-3218
Xiaowen PanDepartment of Endocrinology and Metabolism, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0002-0603-5648
Yu FengDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-0034-6397
Pengfei ShanDepartment of Endocrinology and Metabolism, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0002-6684-9395
Zhuo-Xian MengDepartment of Pathology and Pathophysiology and Department of Cardiology, School of Medicine, Second Affiliated Hospital, Zhejiang University, Hangzhou, China.ORCID 0000-0001-8177-5593
Second Affiliated Hospital of Zhejiang University · CNUniversity of Michigan · USXuzhou Medical College · CNHangzhou First People's Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and type 2 diabetes (T2D) are the leading causes of the progressive decline in muscle regeneration and fitness in adults. The muscle microenvironment is known to play a key role in controlling muscle stem cell regenerative capacity, yet the underlying mechanism remains elusive. Here, we found that Baf60c expression in skeletal muscle is significantly downregulated in obese and T2D mice and humans. Myofiber-specific ablation of Baf60c in mice impairs muscle regeneration and contraction, accompanied by a robust upregulation of Dkk3, a muscle-enriched secreted protein. Dkk3 inhibits muscle stem cell differentiation and attenuates muscle regeneration in vivo. Conversely, Dkk3 blockade by myofiber-specific Baf60c transgene promotes muscle regeneration and contraction. Baf60c interacts with Six4 to synergistically suppress myocyte Dkk3 expression. While muscle expression and circulation levels of Dkk3 are markedly elevated in obese mice and humans, Dkk3 knockdown improves muscle regeneration in obese mice. This work defines Baf60c in myofiber as a critical regulator of muscle regeneration through Dkk3-mediated paracrine signaling.

Indexed as

Diabetes Mellitus, Type 2Paracrine CommunicationAdultAnimalsHumansMiceMice, ObeseMuscle, SkeletalRegeneration

Identifiers

PMID37284884
PMCPMC10250555
OpenAlexW4379598557

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.