Evidence map›Paper›PMID 41580430›Full record

ArticleNature communications2026

Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation.

Zhiyu Feng, Yuan Gao, Han Gao, Siyu Sun, Weilan Na, Xianghui Huang, Shuolin Li, Chaozhong Tan, Shaojie Min, Yuquan Lu and 11 more

Abstract read
PubMed Full text at PMC Publisher
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

21 authors.

Zhiyu Feng *Shanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Yuan Gao *Shanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Han Gao *Shanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Siyu Sun *Shanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Weilan Na *Shanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Xianghui HuangFujian Key Laboratory of Neonatal Diseases, Children's Hospital of Fudan University at Xiamen (Xiamen Children's Hospital), Fujian, China.
Shuolin LiShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Chaozhong TanShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Shaojie MinShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Yuquan LuShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Quannan ZhuangShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Siyi LinShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Xiaojing MaShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China.
Ying LiuHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID http://orcid.org/0000-0001-9447-030X
Weinian ShouHerman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID http://orcid.org/0000-0001-5538-9605
Mei WangShanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jing WangShanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhongkai GuInstitutes of Biomedical Sciences of Fudan University, Shanghai, China.
Wei ShengShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China. sheng4616@126.com.ORCID http://orcid.org/0000-0001-7473-0864
Feizhen WuIntelligent Medicine Institute of Fudan University, Shanghai, China. wufz@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1265-9887
Guoying HuangShanghai Key Laboratory of Birth Defects, Pediatric Heart Center, Children's Hospital of Fudan University, Shanghai, China. gyhuang@shmu.edu.cn.ORCID http://orcid.org/0000-0003-0505-5839

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32070653National Natural Science Foundation of China (National Science Foundation of China) 82200264National Natural Science Foundation of China (National Science Foundation of China) 82270312
6 · The paper itself

Abstract

NONO is recognized as a critical molecular scaffold involved in both transcriptional and posttranscriptional regulation. Mutations in NONO are frequently linked to congenital heart diseases (CHDs) in humans. However, the mechanisms by which NONO regulates cardiac development remain elusive. Here, we identified NONO as a pivotal dual-function regulator of cardiomyocyte differentiation in human induced pluripotent stem cells (hiPSCs). NONO deficiency in hiPSCs results in a distinct defect in early cardiomyocyte differentiation. Mechanistically, NONO interacts with HOXA1 and regulates the dynamic expression of key genes during early cardiomyocyte differentiation. ChIP-seq analysis reveals that NONO loss reduces HOXA1 occupancy at target genes, compromising its transcriptional regulation. Additionally, NONO and HOXA1 cooperatively activate the Wnt signaling. Taken together, these findings establish the NONO-HOXA1-Wnt axis as a key molecular mechanism in cardiomyocyte differentiation and provide insights into the etiology of CHDs associated with NONO mutations.

Identifiers

PMID41580430
PMCPMC12936118

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.