Altered contractility, Ca²⁺ transients, and cell morphology seen in a patient-specific iPSC-CM model of Ebstein’s anomaly with left ventricular noncompaction

Suma K. Thareja,Melissa Anfinson,Matthew Cavanaugh,Min Su Kim,Peter Lamberton,Jackson Radandt,Ryan Brown,Huan-Ling Liang,Karl Stamm, Muhammad Bilal Afzal,Jennifer L. Strande,Michele A. Frommelt,John Lough,Robert H. Fitts,Michael E. Mitchell,Aoy Tomita‐Mitchell

American Journal of Physiology-heart and Circulatory Physiology（2023）

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摘要

We demonstrate here that iPSCs derived from patients with Ebstein’s anomaly and left ventricular noncompaction, when differentiated into cardiomyocytes, display significant structural and functional changes that offer insight into disease pathogenesis, including altered ER/SR and mitochondrial morphology, contractility, and calcium signaling.

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left ventricular noncompaction,ebsteins,altered contractility,anomaly,patient-specific

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Altered contractility, Ca2+ transients, and cell morphology seen in a patient-specific iPSC-CM model of Ebstein’s anomaly with left ventricular noncompaction

Altered contractility, Ca²⁺ transients, and cell morphology seen in a patient-specific iPSC-CM model of Ebstein’s anomaly with left ventricular noncompaction