Evidence map›Paper›PMID 42098143›Full record

ArticleNature communications2026

ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).

Wen Tang, Bowen Lin, Ming Jin, Tianzhen Liu, Jingyi Zhou, Yanhong Jin, Yi Chen, Yanan Zhu, Gonglu Liu, Ping Hu and 15 more

Abstract read
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

25 authors.

Wen Tang *Department of Medical Genetics and Center for Rare Diseases, the Second Affiliated Hospital, and Zhejiang Key Laboratory of Rare Diseases for Precision Medicine and Clinical Translation, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0009-0007-9083-3688
Bowen Lin *State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Ming Jin *Department of Neurology, First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Tianzhen LiuSchool of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Jingyi ZhouSchool of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Yanhong JinSchool of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Yi ChenDepartment of Neurology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yanan ZhuSchool of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou, China.
Gonglu LiuDepartment of Medical Genetics and Center for Rare Diseases, the Second Affiliated Hospital, and Zhejiang Key Laboratory of Rare Diseases for Precision Medicine and Clinical Translation, Zhejiang University School of Medicine, Hangzhou, China.
Ping HuKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Chengyong ShenDepartment of Neurology of the First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0001-8184-8190
Zhuoxian MengDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0001-8177-5593
Guoping PengDepartment of Neurology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Liqun LeiZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Xingxu HuangZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0001-8934-1247
Chenxiao ZhangSchool of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ke ChenSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Guiheng ZhangInstitute of Immunology, and Department of Respiratory Disease of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0001-8765-4530
Xufeng YangDepartment of Laboratory Medicine, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xue LvDepartment of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0002-0275-7360
Adrien RousseauMRC Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, Dundee, UK.ORCID http://orcid.org/0000-0001-8130-5380
Jian YangState Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0002-1964-7061
Zhi-Ying WuDepartment of Medical Genetics and Center for Rare Diseases, the Second Affiliated Hospital, and Zhejiang Key Laboratory of Rare Diseases for Precision Medicine and Clinical Translation, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0003-2106-572X
Ge BaiDepartment of Neurology of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, Hangzhou, China. gebai@zju.edu.cn.
Zhen ZhongDepartment of Medical Genetics and Center for Rare Diseases, the Second Affiliated Hospital, and Zhejiang Key Laboratory of Rare Diseases for Precision Medicine and Clinical Translation, Zhejiang University School of Medicine, Hangzhou, China. zhenzhong@zju.edu.cn.ORCID http://orcid.org/0000-0003-1536-0554

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31871491National Natural Science Foundation of China (National Science Foundation of China) 82071424National Natural Science Foundation of China (National Science Foundation of China) 82325016National Natural Science Foundation of China (National Science Foundation of China) 82450113
6 · The paper itself

Abstract

A critical question in Duchenne muscular dystrophy (DMD) research is whether regulatory mechanisms beyond dystrophin loss contribute to impaired muscle regeneration. Through integrative analysis of proteomics and single-nucleus RNA sequencing database, we identify the upregulation of ANXA11, a gene encoding a Ca²⁺-dependent phospholipid-binding protein, in MYH3⁺ regenerative myofibers from both mdx mice and DMD patients. This upregulation disrupts the maturation of regenerative myofibers, preventing adequate compensation for muscle loss in mdx mice due to dysregulation of the mTOR pathway. Suppression of Anxa11 via genetic knockout or AAV9-mediated knockdown significantly enhanced MYH3⁺ myofiber maturation, accompanied by restored S6 phosphorylation and robust functional muscle recovery in mdx mice. These results establish ANXA11 as a key regulator of muscle regeneration and a potential therapeutic target for DMD.

Indexed as

AnnexinsMuscle, SkeletalMuscular Dystrophy, DuchenneAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, Inbred mdxMice, KnockoutProteomicsRegenerationTOR Serine-Threonine KinasesAnnexinsTOR Serine-Threonine Kinases

Identifiers

PMID42098143
PMCPMC13365423

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.