Evidence map›Paper›PMID 39892862›Full record

ArticleLife sciences2025

Ethanol exposure during differentiation of human induced pluripotent stem cells reduces cardiomyocyte generation and alters metabolism.

Kun Man, Longping Fu, Alicia Lane, Frank Harris, Olivia Reid, Lawrence C Armand, Parvin Forghani, Ronghu Wu, Victor Faundez, Lou Ann Brown and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Life sciences, 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

11 authors.

Kun ManDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Longping FuSchool of Chemistry and Biochemistry and the Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA, USA.
Alicia LaneDepartment of Cell Biology, Emory University, Atlanta, GA, USA.
Frank HarrisDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Olivia ReidDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Lawrence C ArmandDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Parvin ForghaniDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Ronghu WuSchool of Chemistry and Biochemistry and the Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA, USA.
Victor FaundezDepartment of Cell Biology, Emory University, Atlanta, GA, USA.
Lou Ann BrownDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA.
Chunhui XuDepartment of Pediatrics, Emory University School of Medicine and Children's Healthcare of Atlanta, Atlanta, GA, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA. Electronic address: chunhui.xu@emory.edu.

Funding

Alcohol-induced cardiac injury and repair in human induced pluripotent stem cell modelR01AA028527 · NIAAA · EMORY UNIVERSITY · PI XU, CHUNHUI · 2021 to 2025
$1.8M
High-throughput assessment of chemotherapy-induced cardiotoxicity in 3D human cardiomyocytesR21CA285254 · NCI · EMORY UNIVERSITY · PI XU, CHUNHUI · 2024 to 2024
$402k
NCI NIH HHS R21 CA285254NIAAA NIH HHS R01 AA028527
6 · The paper itself

Abstract

Prenatal alcohol exposure increases the risk of congenital heart diseases (CHDs) by disrupting fetal development, yet the mechanisms underlying alcohol-induced cellular and molecular changes in human cardiogenesis remain unclear. This study investigates the effects of ethanol exposure on cardiomyocyte differentiation using human induced pluripotent stem cells (hiPSCs) as a model. Cardiomyocyte differentiation was induced using Wnt signaling molecules, and hiPSCs were treated with ethanol at concentrations of 17, 50, and 100 mM from day 0 to day 12. Ethanol treatment impaired cardiac differentiation efficiency in the early stage (days 5-7) and reduced cell proliferation in the late stage (days 12-13) in a dose-dependent manner, resulting in fewer cardiac progenitors and cardiomyocytes. Additionally, ethanol exposure caused mitochondrial defects, characterized by redox imbalance, reduced membrane potential, and decreased mitochondrial content and cellular respiration. Proteomic analysis revealed downregulation of proteins involved in calcium binding and fatty acid oxidation, a key metabolic pathway for cardiac development. These findings shed light on the mechanisms by which alcohol disrupts cardiomyocyte differentiation and may inform strategies to mitigate alcohol-induced CHD risk.

Indexed as

Cell DifferentiationEthanolInduced Pluripotent Stem CellsMyocytes, CardiacCell ProliferationHumansWnt Signaling PathwayEthanolCardiomyocyte generationCongenital heart diseaseDevelopmental toxicityEthanol exposureHuman induced pluripotent stem cell differentiationMetabolic dysregulation

Identifiers

PMID39892862
PMCPMC11834986

What Socratic holds

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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.