Evidence map›Paper›PMID 41699400›Full record

ArticleJournal of human genetics2026

Vacuolar myopathy caused by CASQ1 p.Asp244His: pathogenic evidence from two unrelated Chinese families.

Xingyu Xia, Milla Laarne, Tonglin Pan, Kexin Jiao, Nachuan Cheng, Bochen Zhu, Meining Diao, Mingshi Gao, Ying Liu, Chongbo Zhao and 2 more

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 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

12 authors.

Xingyu XiaDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Milla LaarneFolkhälsan Research Center, Helsinki, Finland.ORCID http://orcid.org/0000-0001-5690-4779
Tonglin PanDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Kexin JiaoDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Nachuan ChengDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Bochen ZhuDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Meining DiaoDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Mingshi GaoHuashan Rare Disease Center, Shanghai Medical College, Huashan Hospital, Fudan University, Shanghai, China.
Ying LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Chongbo ZhaoDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Zhe ZhaoDepartment of Neurology, Hebei Medical University Third Hospital, Hebei, China. 37800367@hebmu.edu.cn.
Wenhua ZhuDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai, China. whzhu@fudan.edu.cn.ORCID http://orcid.org/0000-0001-8011-0274

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82171398
6 · The paper itself

Abstract

Calsequestrin-1 (CASQ1)-related myopathy is a rare skeletal muscle disorder caused by mutations in CASQ1 gene, which encodes a major calcium-buffering protein of the sarcoplasmic reticulum (SR). It is characterized histopathologically by tubular aggregates or optically empty vacuoles, predominantly affecting type II muscle fibers. In this study, we report two unrelated Chinese patients presenting with late-onset, slowly progressive muscle weakness, fatigue, and myalgia. Both had mildly to moderately elevated serum creatine kinase levels. Muscle biopsies revealed typical optically empty vacuoles primarily in type II fibers. Whole-exome sequencing identified an identical heterozygous CASQ1 variant, c.730G > C (p.Asp244His), located at a highly conserved residue. In vitro expression of the mutant CASQ1 in HeLa cells confirmed its aggregation tendency, suggesting impaired protein folding or calcium handling. Immunofluorescence revealed abnormal aggregation of CASQ1 protein around the edge of vacuoles, co-localized with SQSTM1/p62, and the endoplasmic reticulum (ER) stress marker PERK. Our findings support the pathogenic role of the p.Asp244His variant and provide further insights into CASQ1-related myopathy in Asian populations.

Indexed as

Calcium-Binding ProteinsLysosomal Storage DiseasesMuscular DiseasesAdultCalsequestrinEast Asian PeopleExome SequencingFemaleHeLa CellsHumansMaleMiddle AgedMuscle, SkeletalMutationPedigreeCalcium-Binding ProteinsCalsequestrinCASQ1 protein, human

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.