Evidence map›Paper›PMID 40528267›Full record

ArticleStem cell research & therapy2025

CHD7 regulates definitive endodermal and mesodermal development from human embryonic stem cells.

Rong Hu, Jin Zhao, Kuan Chen Lai, Shikun Wang, Jianqing Zheng, Christopher Stoddard, Laijun Lai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Role of CHD chromatin remodelers in heart development.World journal of pediatrics : WJP · 2026
    Review
  2. [Kallmann syndrome in a girl caused by a novelZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  3. Review
  4. Article
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

7 authors.

Rong Hu *Department of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.
Jin Zhao *Department of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.
Kuan Chen LaiDepartment of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.
Shikun WangDepartment of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.
Jianqing ZhengDepartment of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.
Christopher StoddardDepartment of Department of Genetics and Genome Sciences, University of Connecticut Health, Farmington, CT, USA.
Laijun LaiDepartment of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA. laijun.lai@uconn.edu.ORCID http://orcid.org/0000-0002-4581-7642

Funding

Modeling and treating T cell immunodeficiency in CHARGE syndrome by ESC- and iPSC-derived thymic epithelial cellsR01AI175087 · NIAID · UNIVERSITY OF CONNECTICUT STORRS · PI Laijun Lai · 2023 to 2026
$1.8M
Treating T cell immunodeficiency among older adults by a recombinant Foxn1 fusion proteinR33AG072234 · NIA · UNIVERSITY OF CONNECTICUT STORRS · PI LAI, LAIJUN · 2023 to 2025
$1.4M
NIAID NIH HHS R01 AI175087NIA NIH HHS R33 AG072234NIH HHS R01AI175087NIH HHS R33AG072234
6 · The paper itself

Abstract

backgroundCHD7 encodes an ATP-dependent chromodomain helicase DNA binding protein; mutations in this gene lead to multiple developmental disorders, including CHARGE (Coloboma, Heart defects, Atresia of the choanae, Retardation of growth and development, Genital hypoplasia, and Ear anomalies) syndrome. How the mutations cause multiple defects remains largely unclear. Embryonic definitive endoderm (DE) generates the epithelial compartment of vital organs such as the thymus, liver, pancreas, and intestine.

methodsIn this study, we used the clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technique to delete the CHD7 gene in human embryonic stem cells (hESCs) to generate CHD7 homozygous mutant (CHD7

resultsWe found that deletion of CHD7 led to reduced capacity to develop into DE and mesoderm in a dose-dependent manner. Loss of CHD7 led to significant changes in the expression and chromatin accessibility of genes associated with several pathways. We identified 40 genes that were highly down-regulated in both the expression and chromatin accessibility in CHD7 deleted hESC-DE cells.

conclusionsCHD7 is critical for DE and mesodermal development from hESCs. Our results provide new insights into the mechanisms by which CHD7 mutations cause multiple congenital anomalies.

Indexed as

DNA-Binding ProteinsDNA HelicasesEndodermHuman Embryonic Stem CellsMesodermCell DifferentiationHumansCHD7 protein, humanDNA-Binding ProteinsDNA HelicasesCHARGE syndromeCHD7Definitive endodermHuman embryonic stem cells

Identifiers

PMID40528267
PMCPMC12175391

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.