ArticleAlcohol, clinical & experimental research2023
Chronic ethanol exposure induces mitochondrial dysfunction and alters gene expression and metabolism in human cardiac spheroids.
Article in Alcohol, clinical & experimental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- White Wine Intake Reduces Mitochondrial Complex I-Derived ROS in the Male Rat Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Gastric-protective and antioxidant effects of fermentedOpen life sciences · 2026Article
- A combination of ethanol and arachidonic acid promotes steatosis and endoplasmic reticulum stress and impairs mitochondrial respiration in H9c2 cardiomyoblasts.Lipids in health and disease · 2025Article
- Ethanol Exposure Increases Oxygen Consumption by Developing Cerebral Arteries in a Trimester-, Concentration- and Sex-Dependent Manner.Biomolecules · 2025Article
- Metabolic Modulation in Dilated Cardiomyopathy: From Pathophysiology to Therapy.Reviews in cardiovascular medicine · 2025Review
- Bioactive silver nanoparticles derived from Carica papaya floral extract and its dual-functioning biomedical application.Scientific reports · 2025Article
- Ethanol exposure during differentiation of human induced pluripotent stem cells reduces cardiomyocyte generation and alters metabolism.Life sciences · 2025Article
- Prenatal Alcohol Exposure and Metabolic Disorders in Pediatrics: The Role of the Oxidative Stress-A Review of the Literature.Children (Basel, Switzerland) · 2024Review
- Chronic alcohol-related myopathy: a closer look at the role of lipids.Frontiers in physiology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic alcohol consumption in adults can induce various cardiac toxicities such as arrhythmias, cardiomyopathy, and heart failure. Prenatal alcohol exposure can increase the risk of developing congenital heart defects among offspring. Understanding the molecular mechanisms underlying long-term alcohol exposure-induced cardiotoxicity can help guide the development of therapeutic strategies.
methodsCardiomyocytes derived from human-induced pluripotent stem cells (hiPSC-CMs) were engineered into cardiac spheroids and treated with clinically relevant concentrations of ethanol (17 and 50 mM) for 5 weeks. The cells were then analyzed for changes in mitochondrial features, transcriptomic and metabolomic profiles, and integrated omics outcomes.
resultsFollowing chronic ethanol treatment of hiPSC-CMs, a decrease in mitochondrial membrane potential and respiration and changes in expression of mitochondrial function-related genes were observed. RNA-sequencing analysis revealed changes in various metabolic processes, heart development, response to hypoxia, and extracellular matrix-related activities. Metabolomic analysis revealed dysregulation of energy metabolism and increased metabolites associated with the upregulation of inflammation. Integrated omics analysis further identified functional subclusters and revealed potentially affected pathways associated with cardiac toxicities.
conclusionChronic ethanol treatment of hiPSC-CMs resulted in overall decreased mitochondrial function, increased glycolysis, disrupted fatty acid oxidation, and impaired cardiac structural development.
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