Chronic ethanol exposure induces mitochondrial dysfunction and alters gene expression and metabolism in human cardiac spheroids.

ABSTRACT:

Background

Chronic 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.

Methods

Cardiomyocytes 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.

Results

Following

SUBMITTER: Hwang H 

PROVIDER: S-EPMC10149610 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature