Key result
Melatonin restores contractility and improves the HCM phenotype in MYBPC3-deleted hiPSC-CMs by reducing ROS.
Why the study?
MYBPC3 mutations are the leading cause of hypertrophic cardiomyopathy, but the pathogenesis of the condition required further study.
Reducing reactive oxygen species with melatonin improves the cellular phenotype of hypertrophic cardiomyopathy in a human iPSC-derived cardiomyocyte model.
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Does not support clinical melatonin use in HCM; hypothesis-generating for ROS targeting in preclinical models.
Cao et al. (2025) studied Hypertrophic cardiomyopathy. Melatonin vs. Untreated MYBPC3-deleted hiPSC-CMs was evaluated on Calcium handling capacity, ROS levels, and myocardial contractility. Adding melatonin to MYBPC3-deleted hiPSC-CMs restored calcium handling capacity, decreased ROS levels, and improved myocardial contractility, indicating that reducing ROS improves the HCM phenotype.
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