Evidence map›Paper›PMID 41393511›Full record

ArticleFrontiers in molecular biosciences2025

Ddx3xa mutations drive cardiac defects in a zebrafish model via dysregulation of wnt/β-catenin signaling.

Yu Chen, Mei Lin, Ping Zhu, Haochen Wang, Zhongbei Jiao, Kexing Yi, Xueting Yang, Yingshuo Zhang, Xiaoyan Cai, Wuzhou Yuan and 6 more

Abstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2025. 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

16 authors.

Yu Chen *The Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Mei Lin *The Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Ping Zhu *Guangdong Provincial Key Laboratory of Pathogenesis, Targeted Prevention and Treatment of Heart Disease, Guangzhou Key Laboratory of Cardiac Pathogenesis and Prevention, Guangzhou, China.
Haochen WangThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Zhongbei JiaoThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Kexing YiThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Xueting YangThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Yingshuo ZhangThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Xiaoyan CaiThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Wuzhou YuanThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Yongqing LiThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Zhigang JiangThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Yuequn WangThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Fang LiThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Xiushan WuThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.
Xiongwei FanThe Center for Heart Development, College of Life Science, Hunan Normal University, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Mutations in the DDX3X gene are the primary cause of DDX3X syndrome, with over 800 diagnosed families worldwide. DDX3X is also recognized as a single-gene driver for rare syndromes associated with epilepsy, autism, and developmental disorders. Clinical studies suggest potential links between DDX3X mutations and various cardiac comorbidities. However, there is no report on whether Ddx3xa knockout leads to cardiac phenotypes or whether a zebrafish Methods: A Results: Homozygous knockout ( Discussion: This study provides the first evidence that

Indexed as

cardiac defectsCRISPR/Cas9ddx3xaIWR-1 rescuewnt/β-catenin signalingzebrafish

Identifiers

PMID41393511
PMCPMC12696674

What OpenQuestion holds

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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.