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Ranolazine rescues the heart failure phenotype of PLN-deficient human pluripotent stem cell-derived cardiomyocytes. | LitMetric
Phospholamban (PLN) is a key regulator that controls the function of the sarcoplasmic reticulum (SR) and is required for the regulation of cardiac contractile function. Although PLN-deficient mice demonstrated improved cardiac function, PLN loss in humans can result in dilated cardiomyopathy (DCM) or heart failure (HF). The CRISPR-Cas9 technology was used to create a PLN knockout human induced pluripotent stem cell (hiPSC) line in this study. PLN deletion hiPSCs-CMs had enhanced contractility at day 30, but proceeded to a cardiac failure phenotype at day 60, with decreased contractility, mitochondrial damage, increased ROS production, cellular energy metabolism imbalance, and poor Ca handling. Furthermore, adding ranolazine to PLN knockout hiPSCs-CMs at day 60 can partially restore Ca handling disorders and cellular energy metabolism, alleviating the PLN knockout phenotype of HF, implying that the disorder of intracellular Ca transport and the imbalance of cellular energy metabolism are the primary mechanisms for PLN deficiency pathogenesis.
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