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Cardiomyocytes show hypertrophic growth and remodeling in response to prolonged mechanical stress or abnormal neurohumoral activation.Although the hypertrophic response is initially compensatory, it ultimately causes heart failure, which is a leading cause of morbidity and mortality in the world.Previous studies have showed that nitric oxide (NO), cyclic GMP and protein kinase G (PKG) signaling pathway can inhibit cardiac hypertrophy remodeling process.However, the underlying mechanisms for the anti-hypertrophic effect of NO-cGMP-PKG signals are not fully understood.In the present study, we used human embryonic stem cell-derived cardiomyocytes (hESC-CMs) as the model to explore the mechanism of NO-cGMP-PKG inhibition on human cardiac hypertrophy.