Evidence map›Paper›PMID 41568329›Full record

ArticleFrontiers in genetics2025

Jia Fu, Jing Zhang, Youxian Zhang, Dongming Sun, Kun Xia, Ruigeng Wang, Xiaoyuan Feng, Aiguo Zhai, Yufeng Huang, Xiaobin Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Jia Fu *Department of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jing Zhang *Department of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Youxian Zhang *Department of General Surgery, Hubei Provincial Hospital of Integrated Chinese and Western Medicine, Wuhan, China.
Dongming SunDepartment of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Kun XiaDepartment of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ruigeng WangDepartment of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiaoyuan FengWuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aiguo ZhaiWuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yufeng HuangWuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiaobin LiCollege of Food Science and Engineering, Shannxi University of Science and Technology, Xi'an, China.
Wenjun YuDepartment of Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Yong ZhangDepartment of Cardiology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study aims to elucidate the pathogenicity of the Methods: Protein 3D modeling predicted structural alterations induced by the mutation. Results: Bioinformatic analysis revealed disruption of hydrogen bonding and electrostatic potential at the mutation site. Conclusion: This study establishes a novel link between TPM1-p.E181K and sporadic RCM. We demonstrate that its pathogenesis is mediated through a cascade of events: calcium dyshomeostasis leads to the suppression of CaMKII/HDAC4 phosphorylation, which subsequently causes sarcomere structural disruption, and ultimately results in myocardial hypercontractility. This identified signaling axis may represent a promising therapeutic target for RCM.

Indexed as

CaMKII/HDAC4molecular mechanismspediatric cardiologyrestrictive cardiomyopathyTPM1-p.E181K

Identifiers

PMID41568329
PMCPMC12818787

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.