Evidence mapPaperPMID 37468484Full record

ArticleNature communications2023

The muscle-enriched myokine Musclin impairs beige fat thermogenesis and systemic energy homeostasis via Tfr1/PKA signaling in male mice.

Lu Jin, Shuang Han, Xue Lv, Xiaofei Li, Ziyin Zhang, Henry Kuang, Zhimin Chen, Cheng-An Lv, Wei Peng, Zhuoying Yang and 16 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Brain-muscle axis regulation of neuroinflammation and sarcopenia in Parkinson's disease: the bridging role of lactylation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  10. SEMA3E promotes beige adipocyte differentiation and thermogenesis via β-catenin signaling in mice.Apoptosis : an international journal on programmed cell death · 2026
    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

26 authors at 9 institutions in 2 countries.

Lu Jin *Department of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-0946-3357
Shuang Han *Department of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xue Lv *Department of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-0275-7360
Xiaofei Li *Department of Sport Medicine, The Lianyungang First People's Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of Kangda College of Nanjing Medical University, Lianyungang, China.
Ziyin ZhangDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Henry KuangLife Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, USA.
Zhimin ChenLife Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, USA.
Cheng-An LvDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Wei PengDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhuoying YangDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Miqi YangDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lin MiLife Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, USA.
Tongyu LiuLife Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, USA.
Shengshan MaDepartment of Sport Medicine, The Lianyungang First People's Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of Kangda College of Nanjing Medical University, Lianyungang, China.
Xinyuan QiuDepartment of Biology and Chemistry, College of Science, National University of Defense Technology, Changsha, China.ORCID 0000-0002-9662-8075
Qintao WangDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiaowen PanDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Pengfei ShanDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yu FengDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-0034-6397
Jin LiThe Second Affiliated Hospital, School of Public Health, Zhejiang University School of Medicine, Hangzhou, China.
Fudi WangThe Second Affiliated Hospital, School of Public Health, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-8730-0003
Liwei XieGuangdong Provincial Key Laboratory of Microbial Culture Collection and Application, State Key Laboratory of Applied Microbiology Southern China, Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou, China.ORCID 0000-0002-4747-1753
Xuyun ZhaoDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jun-Fen FuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China. fjf68@zju.edu.cn.ORCID 0000-0001-6405-1251
Jiandie D LinLife Sciences Institute and Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, USA.ORCID 0000-0001-8069-5647
Zhuo-Xian MengDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. zxmeng@zju.edu.cn.ORCID 0000-0001-8177-5593
Second Affiliated Hospital of Zhejiang University · CNUniversity of Michigan · USChildren's Hospital of Zhejiang University · CNHangzhou First People's Hospital · CNXuzhou Medical College · CNGuangdong Academy of Sciences · CNNational University of Defense Technology · CNShanghai Jiao Tong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle and thermogenic adipose tissue are both critical for the maintenance of body temperature in mammals. However, whether these two tissues are interconnected to modulate thermogenesis and metabolic homeostasis in response to thermal stress remains inconclusive. Here, we report that human and mouse obesity is associated with elevated Musclin levels in both muscle and circulation. Intriguingly, muscle expression of Musclin is markedly increased or decreased when the male mice are housed in thermoneutral or chronic cool conditions, respectively. Beige fat is then identified as the primary site of Musclin action. Muscle-transgenic or AAV-mediated overexpression of Musclin attenuates beige fat thermogenesis, thereby exacerbating diet-induced obesity and metabolic disorders in male mice. Conversely, Musclin inactivation by muscle-specific ablation or neutralizing antibody treatment promotes beige fat thermogenesis and improves metabolic homeostasis in male mice. Mechanistically, Musclin binds to transferrin receptor 1 (Tfr1) and antagonizes Tfr1-mediated cAMP/PKA-dependent thermogenic induction in beige adipocytes. This work defines the temperature-sensitive myokine Musclin as a negative regulator of adipose thermogenesis that exacerbates the deterioration of metabolic health in obese male mice and thus provides a framework for the therapeutic targeting of this endocrine pathway.

Indexed as

Adipose Tissue, BeigeAdipose Tissue, WhiteAnimalsHomeostasisHumansMaleMammalsMiceMice, Inbred C57BLMuscle ProteinsMusclesObesityThermogenesisTranscription FactorsMuscle ProteinsOstn protein, mouseTranscription Factors

Identifiers

PMID37468484
PMCPMC10356794
OpenAlexW4384819165

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.