Evidence map›Paper›PMID 42850247›Full record

ArticleNature communications2026

CNIH4 regulates systemic metabolism and exercise adaptations in male mice primarily through the modulation of β-adrenergic receptor trafficking.

Xu Liu, Zhihong Wang, Shuya Chen, Runqi Wang, Tao Bo, Zhiwei Liu, Zhihao Jia, Yong Zhang

Abstract read
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In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Xu Liu *Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China.
Zhihong Wang *Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China.
Shuya ChenJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China.
Runqi WangJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China.
Tao BoKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education, Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID http://orcid.org/0000-0001-9083-4639
Zhiwei LiuJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China.
Zhihao JiaJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China. zhjia@suda.edu.cn.ORCID http://orcid.org/0000-0001-5525-2721
Yong ZhangJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Cambridge-Suda Genomic Resource Center, The Fourth Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, China. yong.zhang@suda.edu.cn.ORCID http://orcid.org/0000-0002-0936-9264

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32100944
6 · The paper itself

Abstract

Exercise improves glucose and lipid metabolism by remodeling skeletal muscle and adipose tissue, processes that depend on beta-adrenergic receptor signaling. How receptor trafficking and activation are coordinated across tissues remains unclear. Here we show that Cornichon homolog 4 controls beta-adrenergic receptor localization and activity in metabolic tissues. Cornichon homolog 4 expression increases in human and mouse skeletal muscle after resistance training. Loss of Cornichon homolog 4 in all tissues or skeletal muscle impairs beta2-adrenergic receptor trafficking and causes exercise-induced hyperglycemia and defective glucose use. Its loss also worsens diet-induced obesity. In adipose tissue, loss of Cornichon homolog 4 weakens beta3-adrenergic receptor signaling, thermogenesis and exercise-induced lipolysis. Pharmacological activation of beta2- or beta3-adrenergic receptors partially restores glucose or adipose defects. Mechanistically, Cornichon homolog 4 links adrenergic receptor signaling to extracellular matrix gene expression and Smad signaling. These findings identify Cornichon homolog 4 as a coordinator of metabolic adaptation.

Indexed as

Adaptation, PhysiologicalPhysical Conditioning, AnimalReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2Adipose TissueAnimalsGlucoseHumansLipolysisMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalObesityProtein TransportGlucoseReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2Receptors, Adrenergic, beta-3

Identifiers

PMID42850247

What OpenQuestion holds

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Registered trials

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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.